I just finished reading health blogger and podcaster, Jimmy Moore's, new book called Cholesterol Clarity: What the HDL is Wrong with My Numbers. For those interested in diving deeper into one of nutrition's most misconstrued and contentious issues, or simply want the "straight dope on cholesterol" (borrowing from the name of Peter Attia's unparalleled blog series on the issue, which I HIGHLY recommend), this is a must read book. Not only does it provide some of the latest research and thinking on the topic through a series of interviews with 28 leading experts in the field, but Moore packages the information in an accessible way for the widest possible audience, whether you're a lipid researcher or someone who just wants to stay healthy.
So, let's dive into some the main issues in the book and some of my key takeaways.
Cholesterol is actually a good thing that plays an irreplaceable role in the body. Bottom line: if you don't have cholesterol, you die. Morbid, but true. Here are a few essential things it does or supports in the body:
When cholesterol is too low, bad things can happen. Based on the important functions listed above, you can probably guess some of the negative things that can happen in the body when cholesterol is too low. For example, cholesterol actually plays a very important role in tissue repair, specifically with stem cell production. As a result, blood vessels can become stiffer - not a good combination with small, dense LDL particles. Research has also shown a close link between low cholesterol and a higher risk of infection, cancer, and a variety of mental side effects, such as depression and a higher likelihood of suicidal behavior.
In fact, research has documented that people with the lowest cholesterol levels actually had the highest rate of death from coronary heart disease and demonstrate a greater risk for some cancers. In addition, this study actually found that almost half of patients hospitalized for heart disease (80% experiencing acute symptoms), had LDL cholesterol levels less than 100 mg/dL, which is the current recommended level by the American Heart Association. As Moore argues, LDL cholesterol (and total cholesterol) are bad predictors of heart disease risk.
Dietary cholesterol doesn't really impact your numbers. The amount of cholesterol from food makes up only about 15-30 percent of your body's total cholesterol. In fact, the overwhelming majority of cholesterol our bodies use - up to 2 grams every day - is actually produced within the body itself, mostly in the liver. Cholesterol is tightly regulated by the body and as Dr. Chris Masterjohn explains in Cholesterol Clarity, "if we eat a lot of cholesterol, our bodies make less of it; if we eat less cholesterol, our bodies make more of it. In most people, the majority of cholesterol that is circulating in the blood is made by their own bodies."
All LDL isn't "bad cholesterol." There are actually two kinds, or patterns, of LDL cholesterol. Pattern A is large and fluffy, regarded by experts as generally harmless. Pattern B, on the other hand, are potentially more dangerous since they are small and dense. Many will say that this measure of particle size and number, or LDL-P, is a much better way of determining risk, than the traditional LDL-C measure that shows up on a standard lipid panel (which is actually a calculated number, not one that's directly measured - more in the next section on this).
Thankfully, there are more and more options available to test for this. One such test is called the NMR LipoProfile test made by the relatively new diagnostic testing company in North Carolina, LipoScience. The test uses NMR technology (which stands for nuclear magnetic resonance and is regarded as one of the best technologies on the market) to actually measure the number of LDL particles in a blood sample.
Of course, certain dietary choices can influence the ratio of Pattern A and Pattern B LDL in the blood, which Moore also flags as quite concerning. He particularly focuses in on the relatively recent trends towards promoting polyunsaturated fats, mostly in the form of vegetable oils (things like canola oil, soybean oil, etc). It is true that there is a fair bit of research showing the effectiveness of polyunsaturated fats (PUFAs) at lowering LDL in the blood. The problem is that PUFAs help achieve this reduction in LDL primarily through decreasing the number of good Pattern A LDL particles, leaving mostly Pattern B. You can see how this can be extremely concerning for heart disease and atherosclerosis risk. One of the best ways to increase the number of good Pattern A particles and decrease the number of Pattern B particles is by eating quality saturated fats from things like coconut, and grass-fed beef and butter.
LDL is actually a calculated number on your standard lipid panel. If there is one number from the standard lipid panel that doctors focus on, along with total cholesterol, it's LDL. The entire statin-prescribing system, argues Moore, has been built upon artificially defining a certain threshold for LDL and total cholesterol (which isn't really rooted in any solid evidence as mentioned above) and teaching physicians (very well) to automatically prescribe the drug once your numbers exceed these thresholds. Usually any conversation about diet is secondary or nonexistent. This is essentially how Lipitor and other statin drugs have become some of the most commonly prescribed medication on Earth.
Among some alternatives, like testing for LDL particle size and number, there is also pretty strong consensus that your ratio of HDL cholesterol to triglycerides is a better gauge of current heart health. Both numbers are on the standard lipid panel, which makes them a bit more accessible. The easiest prescription to maximize HDL while minimizing triglycerides is by avoiding carbohydrates and eating more fats.
Keeping total cholesterol low, as guidelines recommend, is 100% counter-intuitive. The prevailing guidelines by a variety of public health authorities focus exclusively on total cholesterol and LDL, and specifically keeping these two numbers low. In the case of total cholesterol, guidelines suggest this number should be kept under 200. But the irony of all of this is that if you're trying to keep total cholesterol low, you're assuming all components that make up the total should be kept to a minimum.
Most people know this is hardly the case. As I mentioned, having a lot of large, fluffy Pattern A LDL particles is not nearly as harmful as having a lot of Pattern B. Also, when it comes to HDL cholesterol, or the so-called "good" kind, every leading health authority suggests we need to keep this number as high as possible. This seems like a big contradiction to say keep some cholesterol particles, like HDL, high, while applying an arbitrary cap to total cholesterol.
Statins do a lot more harm than good. Though statins do lower LDL cholesterol (which I hope I've already convinced you is not necessarily a good thing), here are a few examples of the documented negative consequences of taking statins:
This book is definitely for everyone. I thoroughly enjoyed the balance struck between offering practical guidance while underpinning it all with sound science. If you're trying to cut through all the noise out there on cholesterol or you're interested in tracking your own health and wellness, this is definitely worth the read. My only critique - but this is coming from a researcher who loves evidence - is the lack of citations in the book. Moore does provide some suggested references for additional reading, but I personally could've really benefited from the book to a greater degree with citations, particularly for many of the chapters discussing the science.
Nonetheless, I highly recommend taking a look at this book. It'll definitely challenge (and maybe even change) the way you think about cholesterol.
Note: I was not compensated in anyway for writing this posting. Views are my own.
So, let's dive into some the main issues in the book and some of my key takeaways.
Cholesterol is actually a good thing that plays an irreplaceable role in the body. Bottom line: if you don't have cholesterol, you die. Morbid, but true. Here are a few essential things it does or supports in the body:
- Hormone production, including estrogen, progesterone, testosterone, pregnenolone, adrenaline, cortisol, and DHEA
- The health and efficiency of cell membranes
- Nervous tissue, including the white matter in your brain
- Optimal adrenal gland function, which modulate a number of different vital hormones like adrenaline as well as kidney function
- Water and electrolyte balance
- Formation of Vitamin D
- Immune function
When cholesterol is too low, bad things can happen. Based on the important functions listed above, you can probably guess some of the negative things that can happen in the body when cholesterol is too low. For example, cholesterol actually plays a very important role in tissue repair, specifically with stem cell production. As a result, blood vessels can become stiffer - not a good combination with small, dense LDL particles. Research has also shown a close link between low cholesterol and a higher risk of infection, cancer, and a variety of mental side effects, such as depression and a higher likelihood of suicidal behavior.
In fact, research has documented that people with the lowest cholesterol levels actually had the highest rate of death from coronary heart disease and demonstrate a greater risk for some cancers. In addition, this study actually found that almost half of patients hospitalized for heart disease (80% experiencing acute symptoms), had LDL cholesterol levels less than 100 mg/dL, which is the current recommended level by the American Heart Association. As Moore argues, LDL cholesterol (and total cholesterol) are bad predictors of heart disease risk.
Dietary cholesterol doesn't really impact your numbers. The amount of cholesterol from food makes up only about 15-30 percent of your body's total cholesterol. In fact, the overwhelming majority of cholesterol our bodies use - up to 2 grams every day - is actually produced within the body itself, mostly in the liver. Cholesterol is tightly regulated by the body and as Dr. Chris Masterjohn explains in Cholesterol Clarity, "if we eat a lot of cholesterol, our bodies make less of it; if we eat less cholesterol, our bodies make more of it. In most people, the majority of cholesterol that is circulating in the blood is made by their own bodies."
All LDL isn't "bad cholesterol." There are actually two kinds, or patterns, of LDL cholesterol. Pattern A is large and fluffy, regarded by experts as generally harmless. Pattern B, on the other hand, are potentially more dangerous since they are small and dense. Many will say that this measure of particle size and number, or LDL-P, is a much better way of determining risk, than the traditional LDL-C measure that shows up on a standard lipid panel (which is actually a calculated number, not one that's directly measured - more in the next section on this).
Thankfully, there are more and more options available to test for this. One such test is called the NMR LipoProfile test made by the relatively new diagnostic testing company in North Carolina, LipoScience. The test uses NMR technology (which stands for nuclear magnetic resonance and is regarded as one of the best technologies on the market) to actually measure the number of LDL particles in a blood sample.
Of course, certain dietary choices can influence the ratio of Pattern A and Pattern B LDL in the blood, which Moore also flags as quite concerning. He particularly focuses in on the relatively recent trends towards promoting polyunsaturated fats, mostly in the form of vegetable oils (things like canola oil, soybean oil, etc). It is true that there is a fair bit of research showing the effectiveness of polyunsaturated fats (PUFAs) at lowering LDL in the blood. The problem is that PUFAs help achieve this reduction in LDL primarily through decreasing the number of good Pattern A LDL particles, leaving mostly Pattern B. You can see how this can be extremely concerning for heart disease and atherosclerosis risk. One of the best ways to increase the number of good Pattern A particles and decrease the number of Pattern B particles is by eating quality saturated fats from things like coconut, and grass-fed beef and butter.
LDL is actually a calculated number on your standard lipid panel. If there is one number from the standard lipid panel that doctors focus on, along with total cholesterol, it's LDL. The entire statin-prescribing system, argues Moore, has been built upon artificially defining a certain threshold for LDL and total cholesterol (which isn't really rooted in any solid evidence as mentioned above) and teaching physicians (very well) to automatically prescribe the drug once your numbers exceed these thresholds. Usually any conversation about diet is secondary or nonexistent. This is essentially how Lipitor and other statin drugs have become some of the most commonly prescribed medication on Earth.
Among some alternatives, like testing for LDL particle size and number, there is also pretty strong consensus that your ratio of HDL cholesterol to triglycerides is a better gauge of current heart health. Both numbers are on the standard lipid panel, which makes them a bit more accessible. The easiest prescription to maximize HDL while minimizing triglycerides is by avoiding carbohydrates and eating more fats.
Keeping total cholesterol low, as guidelines recommend, is 100% counter-intuitive. The prevailing guidelines by a variety of public health authorities focus exclusively on total cholesterol and LDL, and specifically keeping these two numbers low. In the case of total cholesterol, guidelines suggest this number should be kept under 200. But the irony of all of this is that if you're trying to keep total cholesterol low, you're assuming all components that make up the total should be kept to a minimum.
Most people know this is hardly the case. As I mentioned, having a lot of large, fluffy Pattern A LDL particles is not nearly as harmful as having a lot of Pattern B. Also, when it comes to HDL cholesterol, or the so-called "good" kind, every leading health authority suggests we need to keep this number as high as possible. This seems like a big contradiction to say keep some cholesterol particles, like HDL, high, while applying an arbitrary cap to total cholesterol.
Statins do a lot more harm than good. Though statins do lower LDL cholesterol (which I hope I've already convinced you is not necessarily a good thing), here are a few examples of the documented negative consequences of taking statins:
- This 2013 article found a 21% increased risk of death among women with breast cancer who took statins compared to those who didn't. Other studies have documented the link between statin use and musculoskeletal diseases and joint pain.
- Compared to people who did not use statins, statin users had had a 50% increased risk for any musculoskeletal pain, a 59% increased risk for lower back pain, and a 50% increased risk for lower extremity pain.
- This review article documents the ample evidence showing increased risk of cardiovascular disease in women among statin users, including a three-fold increase in risk of coronary artery and aortic artery calcification.
- Statin use has been shown to hinder the positive effects of exercise among overweight and obese individuals.
It's all about inflammation. If there is one thing to worry about instead of cholesterol, Moore
argues, we should be much more concerned about inflammation in the body
and the things that cause it. This is the true cause of atherosclerosis.
In his words, "without inflammation, cholesterol can't harm you." It's really all about cholesterol oxidation, which is nearly a two-fold better predictor of heart disease risk than simply looking at cholesterol alone. So,
we should be focusing more on things that cause chronic inflammation in
the body, which results from poor diet, smoking, lack of sleep,
infrequent exercise, elevated stress, and a compromised gut, just to
name a few that Moore references. One of the best blood markers for
determining the amount of chronic inflammation in the body is something
called high-sensitivity C-reactive protein, or hs-CRP. Many experts have
argued that hs-CRP is a much better biomarker to track because it's a
much better predictor of heart disease and health complications than
total cholesterol or LDL.
****
Nonetheless, I highly recommend taking a look at this book. It'll definitely challenge (and maybe even change) the way you think about cholesterol.
Note: I was not compensated in anyway for writing this posting. Views are my own.
http://www.carbsmart.com/5-health-markers-that-matter-more-than-total-cholesterol-and-ldl-c.html
ReplyDelete3. LDL-P: LDL Particle number
There’s still some debate amongst the cholesterol experts about whether it is the total number of particles or the size of the particles that matters most. Since the science isn’t settled on this, we present both sides of that argument in Cholesterol Clarity and let the reader decide for themselves which side they choose to believe.
If you search on 6 Month Lipid Panel for Jimmy Moore you should find his latest update before this book.
http://livinlavidalowcarb.com/blog/6-month-lipid-panel-update-on-my-nutritional-ketosis-n1-experiment/16449
In comments, Thomas Dayspring wrote... "Dr Lipid analysis: Using all the knowledge we possess today, all of the numbers that you are thrilled about have no meaning in the face of a 99th percentile LDL-P. You also should not say an LDL-C of 285 has no meaning. The cholesterol concentrations that often have no meaning are low levels (where an LDL-P is needed to evaluate risk). No one with an LDL-C of 285 with the exception of a Type III dyslipoproteinemia patient have a low apoB or LDL-P. If you have an LDL-C that high, particle testing is not needed. You need to significantly reduce the saturated fat in your diet and see what happens: repeat the NMR in 3 weeks and you will know if your nightmare LDL-P is sat fat related. I'll bet your LDL-P drops. If it does not, you need serious lipid-modulating medication. We have seen this paradoxical horrific rise in LDL-P in some people who are on ketotic diets."
Yet here is the quote Jimmy chose for Dayspring in his chapter on LDL particles (Chapter 9):
"The least accurate way of estimating your atherogenic risk on a standard cholesterol panel would be to look at total cholesterol or LDL cholesterol."
Does this seem like an accurate reflection of Dayspring's full positions on the topic? This chapter should have contained liberal quoting from Dayspring, yet Jimmy Moore claimed on his blog that "I let him make his case in my book."
4. Small LDL-P: Small LDL Particle number
The Small LDL-P begins to become much more problematic when this number comprises more than 20 percent of your total LDL particles. For example, if your LDL-P is 1000, then your Small LDL-P needs to be 200 or less. Not to sound like a broken record, but if you consume less carbohydrates to your own personal tolerance level, and eat more healthy
saturated and monounsaturated fats in your diet, then your Small LDL-P will go down.
His small LDL-P percentage has gone UP from 6.4% to 17.5% between 10/12 and 4/13
He claims that TC and LDL are virtually irrelevant yet in his book he says
Cholesterol Clarity Testing Guide with Optimal Ranges
Standard Lipid Panel
Total Cholesterol Mostly irrelevant, but women should be 250 mg/dL or below and men should be 220 mg/dL or below
LDL-C 130 mg/dL or below, but higher levels are not necessarily relevant to your heart health risk.
HDL-C Above 50mg/dL is good, but 70 mg/dL or higher is best
VLDL-C Between 10 and 14 mg/dL
Triglycerides 100 mg/dL or below, but under 70mg/dL is best
Non-HDLCholesterol No evidence of an optimal level
Here's a very good review from the other point of view
http://www.amazon.com/Cholesterol-Clarity-What-Wrong-Numbers/product-reviews/1936608383/ref=sr_cr_hist_1?ie=UTF8&filterBy=addOneStar&showViewpoints=0
Your thoughts
http://www.lecturepad.org/dayspring/lipidaholics/pdf/LipidaholicsCase291.pdf
ReplyDeleteLet’s get rid of the nonsense seen all over the internet that atherosclerosis is an inflammatory disease, not a cholesterol disease. That is baloney-with the reality being that it is both. One cannot have atherosclerosis without sterols, predominantly cholesterol being in the artery wall: No cholesterol in arteries – no atherosclerosis. Plenty of folks have no systemic vascular inflammation and have atherosclerotic plaque. However clinicians have no test that measures cholesterol within the plaque – it is measured in the plasma. It is assumed, that if total or LDL-C or non-HDL-C levels are elevated the odds are good that some of that cholesterol will find its way into the arteries, and for sure there, are many studies correlating those measurements with CHD risk. Yet, we have lots of patients with very low TC and LDL-C who get horrific atherosclerosis. We now recognize that the cholesterol usually gains arterial entry as a passenger inside of an apoB-containing lipoprotein (the vast majority of which are LDLs) and the primary factor driving LDL entry into the artery is particle number (LDL-P), not particle cholesterol content (LDL-C). Because the core lipid content of each and every LDL differs (how many cholesterol molecules it traffics) it takes different numbers of LDLs to traffic a given number of cholesterol molecules: the more depleted an LDL is of cholesterol, the more particles (LDL-P) it will take to carry a given cholesterol mass (LDL-C). The usual causes of cholesterol depleted particles are that the particles are small or they are TG-rich and thus have less room to carry cholesterol molecules. Who has small LDLs or TG-rich LDL's? – insulin resistant patients! After particle number endothelial integrity is certainly related to atherogenic particle entry: inflamed endothelia have inter-cellular gaps and express receptors that facilitate apoB-particle entry. So the worse scenario is to have both high apoB and an inflamed dysfunctional endothelium. Is it better to have no inflammation in the endothelium – of course! But make no mistake the driving force of atherogenesis is entry of apoB particles and that force is driven primarily by particle number not arterial wall inflammation: please see Ira Tabas, Kevin Jon Williams, Jan Borén. Subendothelial Lipoprotein Retention as the Initiating Process in Atherosclerosis Update and Therapeutic Implications Circulation. 2007;116:1832-44.