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The LDL Particle Size Argument: Do We Understand This Correctly?

Answered on September 12, 2014
Created July 12, 2011 at 12:57 AM

Some people explain away their high LDL by invoking the particle size argument. Those who do low-carb Paleo typically have low triglycerides, which correlate well with Pattern A -- the large, bouncy and fluffy LDL type thought to be harmless. But is that really the case? I remember actually reading from the Healthy Skeptic blog that the large LDL particles protect one from the risk of heart disease.

Well, I was listening to an interview with William Castelli, who led the Framingham Heart Study for many years. For all intents and purposes, this guy is the face of Conventional Medicine and is Mr. Mainstream Cardiology. Affiliated with 3 medical schools, he is now retired and heads a wellness program in Framingham, MA. He differs with the notion that the large particle size "protects" one from heart disease.

The interview can be read here:

http://www.prescription2000.com/Interview-Transcripts/2011-02-18-william-castelli-heart-disease-lipids-transcript.html

and heard here:

http://www.prescription2000.com/Staying-Healthy-Today-Radio-Interviews/2011-02-18-william-castelli-heart-disease-lipids.html

=========================

Here are Dr. Castelli's main points:

  • Large particle size LDLs go into artery walls at a slower rate than the small and dense LDLs, which go in at 3 times the rate.

  • If your large LDL is elevated, it causes more heart attack (twice actually) than the low LDL level composed of the same particle type.

  • The small, dense LDL is three times more dangerous than the equivalent level of the large LDL.

  • The particle size is largely determined by triglycerides: As your triglycerides dip below 60, the large size predominates. As triglycerides exceed 150, the "wrong", smaller ones predominate (also, the HDL type isn't the best either at this point -- there're apparently 12 different HDL types that fluctuate depending on triglyceride and other levels).

  • To lower your triglycerides, you should remove refined carbohydrates (ice cream, white flour, cookies, sugar). Notice here he does not mention starch, only processed carbs (I happen to think unprocessed starch will also raise trigs). No argument though from the Paleo crowd.

So what are we to take away from this interview? Dr. Castelli's position is as follows:

  • The large LDL type is certainly less dangerous, but it's not "safe". At least, that's what Mainstream Medicine believes. He seems to cite relevant studies (Lamark's Quebec study, Berkeley, etc.) to support his position.

  • The large LDL type does not protect you from a cardiac event, as claimed. The cardiac risk is just lower.

  • It is desirable to keep LDL low, no matter what the particle size.

  • It is also desirable to keep triglycerides below 60, to lower the relative risk of LDL deriving from the worse particle size (Type B). In other words, A is better than B, but both are bad. You want to minimize both, if you can help it.

==================

Are you in agreement with these? I don't have any set position; I'm open-minded and skeptical about the cholesterol risk but also feel that the particle size argument is a smokescreen and could backfire.

What if you find out that your particle type is A. But what if Mr. Primary Care Physician quotes the above argument verbatim in pushing statin medication (which Dr. Castelli wholly approves of)? What will you say to get him off your back?

B2f2d854c1f60630089ba6f413618868

(0)

on May 26, 2012
at 10:17 PM

Chris is far from a layman. He is a PhD candidate in nutritional sciences with a concentration in biochemical and molecular nutrition. He has two peer reviewed papers that can be found on pub med.

3c6b4eed18dc57f746755b698426e7c8

(5152)

on March 20, 2012
at 06:21 AM

I have a little different take on this. I've gone on a 60% carb diet, after having done 20% carb, 60% fat and 20% prot. My TC did fall from 225 to 160; so that part is true ... however, my TG did increase to 115 from 90. The part that fell was the LDL: from 110 to 80. I definitely think that in some subgroup (possibly ApoE4 or ApoE2), LDL WILL fall by consuming more whole food carbs and cutting fat.

Ed71ab1c75c6a9bd217a599db0a3e117

(25472)

on September 05, 2011
at 02:29 AM

Dr. Caldwell Esselstyn is at the Cleveland clinic, a retired general surgeon with zero nutrition training but huge ties to the vegan community and their agenda. Major fucking pass from me. This guy is going to kill many people. Him and ornish are in bed together. Once jobs and clinton die we will see how this goes.

Ed71ab1c75c6a9bd217a599db0a3e117

(25472)

on September 05, 2011
at 02:26 AM

Lol at those last two statements. I completely believe the opposite

Bcad307b240275ae3f5820ba6eb4a712

(923)

on September 04, 2011
at 07:07 PM

What do your strawmen about hamburgers, cheeese pizzas, and standard American food have to do with paleo dietary philosophy?

928331b87bfa52da4c521d73ef79927b

(40)

on September 04, 2011
at 05:34 PM

Are you kidding me? Chris is not even a doctor! Why someone would even waste their time listening or reading something from this person is beyond me! You have countless of established / trained medical professionals that have peer reviewed studies released. And you want to put your life in the hands of some layman?

Be1dbd31e4a3fccd4394494aa5db256d

(17969)

on July 13, 2011
at 06:29 PM

There will be a way to figure out. Give it some time at low inflammation, good antioxidant status, and high fat, and then check the amount of oxLDL. I'm not convinced that lots of LDL necessarily means lots of oxLDL. Although in people eating normal diets it might look like that, so I think I know where some people are coming from, I just don't agree that it applies to all situations.

Af1d286f0fd5c3949f59b4edf4d892f5

(18472)

on July 13, 2011
at 06:00 PM

This is a good discussion guys. Because even if I test for ApoE, and find that I am type 4, which means eating fat increases LDL for me, I wouldn't want to jump to the conclusion that naturally having a higher LDL is 'bad'. What if it's more true to say that's it's 'necessary' for me to have the higher LDL transports if I choose to eat a higher amount of fat. Most other Paleos I've seen are also able to get their HDL up prety high too though. To me, if I had a very robust HDL, I probably wouldn't feel like I had much to be concerned about.

Be1dbd31e4a3fccd4394494aa5db256d

(17969)

on July 13, 2011
at 05:45 AM

What you suggested is also possible. Whether or not those people would necessarily be better off with lower LDL is hard to say. Kurt Harris had a post a while ago questioning whether or not these people actually needed to try to lower their levels if their inflammation was low and their arteries were healthy. I don't know about that one, but I'll certainly consider it.

Be1dbd31e4a3fccd4394494aa5db256d

(17969)

on July 13, 2011
at 05:44 AM

It isn't just nutrient deficiencies but anything that damages the arteries. It is very plausible that we have a large percentage of the population with severely damaged arteries. Dietary changes to include more coconut and butter will increase cholesterol levels if there is a need for cholesterol. Someone starting a paleo diet with damaged arteries from deficiencies and everything else that damaged them would need a lot of cholesterol. If they failed to increase levels of those nutrients or resolve all of their inflammation then their levels would remind elevated.

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 13, 2011
at 05:07 AM

But even Dr. Lustig attested to this. See my prior post regarding ApoE. For 25% of the population, high fat leads to high cholesterol. Doesn't this seem a bit more plausible: that the 1/4 of the population just don't do well on a high fat diet because of they're type 4s? And we have lots of them! Than that we have a mass epidemic of Cu, I, and choline deficiency affecting the general population? Paul's point seems sound and reasonable but I'm not so sure at the population level whether the deficiency is due to an abrupt dietary change (as it seems to have been for Larry, according to Paul).

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 13, 2011
at 05:04 AM

Stabby, PHD cited deficiencies in copper, choline and even iodine as possibly causing arterial damage, which would then increase LDL. That seems plausible among Paleos who've changed their diets but the above Quebec study involved a whole cross section of male population, some of whom would suffer from familial cholesterolimia. For them, if you eat fat, your chol would go up. (Whether they should be on a low fat diet is another question; I'm not sure).

21fd060d0796fdb8a4a990441e08eae7

(24543)

on July 13, 2011
at 02:55 AM

What is at fault is the discussion sections of papers stemming from Framingham, not the data in and of itself. There are like a billion of these papers in various journals, so you can't generalize, as well as dozens of authors. But by large, they fall into the same trap that biostatisticians figured out decades ago: correlation does not mean causation, and cohort studies are meant to be hypothesis generating and not the backbone of a national agenda. I can't fault them too much for it--very few academic researchers are actually evil. The professors at my school fully believe what they say.

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 13, 2011
at 01:17 AM

Dr. K, I think you're talking about the opportunists and the pharma industry. Sure, there are MDs in the medical-pharma complex. But I don't see evidence of Castelli and Levy overstating what they found, based on just the article read. Grundy, I do not know but those who conducted the study seem to be more or less reasonable.

6120c989fd5b69f42a0834b69b87955b

(24553)

on July 13, 2011
at 01:16 AM

I went and did more reading, and it looks like I had been oversimplistic in my own understanding of how plaque builds up. Apparently, the endothelium is more like a window screen than a stainless steel countertop, and plaque also builds up behind it. Wouldn't all the PUFA in a vegan diet oxidize and cause more problems. I definitely welcome anyone with more understanding of this to chime in here, I'm still learning.

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 13, 2011
at 01:11 AM

So LDL is not THE factor, that's obvious and no one, not the Farmingham authors, is disputing that. The strongest factor is age, since it's no brainer. All people die. In the U.S. around the 80s, most people died from 2 things: CVD or cancer. If you died from cancer, does that imply you didn't have CVD? No, cancer just killed you off sooner. There is a limitation in interpretation and I think some of you are making wild inferences without reading the text.

Ed71ab1c75c6a9bd217a599db0a3e117

(25472)

on July 13, 2011
at 01:10 AM

The opinions from Framingham of why we have statin nation what Framingham really found was not important to the opinion makers in big pharma's pocket.

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 13, 2011
at 01:08 AM

The authors point out that these variables are overlapping, which could be misleading when trated separately. Obesity is related to lack of exercise, which is related to onset of diabetes which is related to age. As separate variables their significance is somewhat understated than whey they're seen as a whole, which contribute to the overall CVD risk. In other words, you might not get significant relatioship in LDL with CVD if you don't smoke, are not obese, are not diabetic, have high HDL, are not of certain age, etc. But if some of these are true, it may be another story.

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 13, 2011
at 12:52 AM

Based on the 2nd article, the authors (Castelli, Levy and Anderson) freely admit that heart disease is a "multifactorial disorder" -- no independent variable captures strong association other than age, smoking or not, and HDL. But as a whole, when you pile these things up, they amount to strong correlation. This is just a review article; no separate analysis is presented and no conclusion is drawn other than the obvious: CVD has many variables, not one smoking gun but many smoking guns which, in totality, add up. Like life, CVD is complex. What else did the authors say?

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 13, 2011
at 12:41 AM

There is so much noise floating around and it's hard to discern who's telling the truth. This is why you have to actually read the articles yourself, to see who's really telling the truth. I only have access to the abstract for the first link. The second article seems open and reasonable: I don't really see any bias in interpreting what the study found.

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 13, 2011
at 12:39 AM

No, Kamal, it seems that Dr. K is saying that those who interpreted the Framingham study did so misleadingly. The study itself does not seem to be misleading. They freely admit what they found -- what was statistically significant or not.

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 12, 2011
at 09:47 PM

If you want your arteries totally shiny and slippery, no plaques, you have to practice veganism! At least that's what the vegans say. If you are a vegan and your cholesterol is below 150, you have no plaque. Again, I'm quoting Dr. Castelli and some vegans. I do not know if that's true.

Be1dbd31e4a3fccd4394494aa5db256d

(17969)

on July 12, 2011
at 03:28 PM

So basically I'm saying that just because you can find a correlation between elevated LDL and heart disease in a population, that doesn't mean that all increases in LDL are bad in all cases. LDL that is indicative of arterial damage is not the same as LDL indicative of someone with the phenotype that produces higher LDL from eating a lot of butter.

Be1dbd31e4a3fccd4394494aa5db256d

(17969)

on July 12, 2011
at 03:20 PM

To simplify, you say "have high overall LDL and ApoB, which promote atherosclerosis over a longer term" do they themselves inherently promote atherosclerosis or is it that in general in a population that tends to eat a bad diet you will find an association between these things in a population? This is the correlation=causation fallacy and it is an incorrect extrapolation.

Be1dbd31e4a3fccd4394494aa5db256d

(17969)

on July 12, 2011
at 03:17 PM

Ok Namby I see your point, and I am saying that any associated between "elevated" LDL is probably caused by the cases with the metabolic syndrome and arterial damage, so it makes no sense to extrapolate to paleos with LDL of 150 and say they need to get it to 100, which is the discussion. There are big differences between people around here. In a normal population you don't have people eating in such a way to try to elevate their LDL with coconut oil and butter and such, that is completely different from those with lots of arterial damage, and so we shouldn't compare them.

Be1dbd31e4a3fccd4394494aa5db256d

(17969)

on July 12, 2011
at 03:16 PM

Ok Namby I see your point, and I am saying that any associated between "elevated" LDL is probably caused by the cases with the metabolic syndrome and arterial damage, so it makes no sense to extrapolate to paleos with LDL of 150 and say they need to get it to 100, which is essential the relevant. There are big differences between people around here. In a normal population you don't have people eating in such a way to try to elevate their LDL with coconut oil and butter and such, that is completely different from those with lots of arterial damage, and so we shouldn't compare them

Be1dbd31e4a3fccd4394494aa5db256d

(17969)

on July 12, 2011
at 03:15 PM

Ok Namby I see your point, and I am saying that any associated between "elevated" LDL is probably indicative of the metabolic syndrome and arterial damage, so it makes no sense to extrapolate to paleos with LDL of 150 and say they need to get it to 100, which is essential the relevant. There are big differences between people around here. In a normal population you don't have people eating in such a way to try to elevate their LDL with coconut oil and butter and such, that is completely different from those with lots of arterial damage, and so we shouldn't compare them.

Be1dbd31e4a3fccd4394494aa5db256d

(17969)

on July 12, 2011
at 03:14 PM

Ok Namby I see your point, and I am saying that any associated between "elevated" LDL is probably indicative of the metabolic syndrome and arterial damage, so it makes no sense to extrapolate to paleos with LDL of 150 and say they need to get it to 100, which is essential the relevant conversation here.

D1c02d4fc5125a670cf419dbb3e18ba7

on July 12, 2011
at 03:06 PM

You might want to look at Chris Masterjohn's blog (The Daily Lipid) since I believe he has written about this. Also check out this podcast with him. In the comments section, there is some discussion about oxLDL also - http://thehealthyskeptic.org/the-healthy-skeptic-podcast-episode-11 Finally, here are some links from Stephan Guyenet- http://wholehealthsource.blogspot.com/2009/07/diet-heart-hypothesis-oxidized-ldl-part.html http://wholehealthsource.blogspot.com/2009/08/diet-heart-hypothesis-oxidized-ldl-part.html

44348571d9bc70c02ac2975cc500f154

(5853)

on July 12, 2011
at 10:01 AM

I keep my arteries happy with daily serving of good fish, better than beef me thinks :) HDL is now over 105, but my tc is too high i think, something must be wrong. Its like 460. I would like to see it somewhere around 250

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 12, 2011
at 06:37 AM

Jack, HDL is your Roto Rooter and way more important than your LDL level or particle size. Get that high if you can. If you can't, check your ApoE status and see if you might be more compatible with a high- or low-fat diet.

Af1d286f0fd5c3949f59b4edf4d892f5

(18472)

on July 12, 2011
at 06:29 AM

some interesting points stabby. in Oct 2010, I had low CRP with similar numbers, so it would seem that inflammation is not an issue for me.but then again, my HDL is super low for the amount of eggs and coconut oil and butter i eat. most paleo folk with so called 'high LDL' also sport a more impressive HDL figure of 60-100 or so. what's a brother gotta do to raise his HDL? drink coconut oil like a cocktail?

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 12, 2011
at 06:22 AM

Even though the conclusion is made regarding association, the benchmark is "increased risk from teh baseline". There is relative risk with elevation in type A LDL level. In other words, MORE of A is BAD. I think that's exactly what Castelli is saying.

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 12, 2011
at 06:18 AM

Castelli actually cites this study: Lamarche, not Lamarck. Those with elevated type A LDL have twice the risk as those with nonelevated type A LDL. If you go to Discussion, it says that those w/high type A LDL levels also have high overall LDL and ApoB, which promote atherosclerosis over a longer term. 260A is not LDL level but the particle size in Angstrom, a nanodistance.

Be1dbd31e4a3fccd4394494aa5db256d

(17969)

on July 12, 2011
at 04:54 AM

Ah right, maybe I'll steam my fish and cover them with spices.

21fd060d0796fdb8a4a990441e08eae7

(24543)

on July 12, 2011
at 04:49 AM

Do you mean to say that we have bigger fish to poach? Because frying a big fish could be bad for your cholesterol. And big fish have more mercury than small fish. Other than that, all good points. Except that associations in cohort data are still quite susceptible to misinterpretation due to confounders. I must admit though, my attitude towards studies is way more laissez faire when the condition being studied doesn't apply to me. If I had super high cholesterol, my views might be very different.

21fd060d0796fdb8a4a990441e08eae7

(24543)

on July 12, 2011
at 04:40 AM

N. Pamby-- the Cordain bit was just an analogy :)

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 12, 2011
at 04:06 AM

W/regard to Cordain, I don't think he really changed his position and you can't say his SFA position is "wrong". He said that SFA causes plaques. The current debate is no longer the existence of plaques but what will instigate a cardiac event: i.e., inflammation. But is SFA atherogenic? I think so, even those Inuits have plaques, according to Cordain.

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 12, 2011
at 04:01 AM

Kamal, correct, the 99% confidence Castelli cites is from the Berkeley study, not the Framingham study. But he readily admits that he missed the importance of triglycerides early and kicks himself for it. What the Framingham study found is the additional correlation between the number of LDL particles (not particle type and not LDL level) and triglycerides. The higher # of LDL particles ==> high triglycerides. What is indisputable is the importance of HDL: i.e., Total Cholesterol / HDL < 3.5 if you can help it. This is not what many (incl. Castelli) expected. Yet they had to embrace this.

21fd060d0796fdb8a4a990441e08eae7

(24543)

on July 12, 2011
at 02:58 AM

Yes. Framingham is way misleading, obviously. But what specifically does this have to do with LDL particle size?

21fd060d0796fdb8a4a990441e08eae7

(24543)

on July 12, 2011
at 02:56 AM

Believe it or not, people can say different things at different times. Not everything a Framingham author says for perpetuity is based on Framingham study data. In fact, almost nothing Dr. Castelli says above is based on Framingham. It's like if I saw a posting about Loren Cordain and said "Don't believe anything he says about indigenous diets...his view on saturated fat was wrong."

Ed71ab1c75c6a9bd217a599db0a3e117

(25472)

on July 12, 2011
at 02:26 AM

Dr Castelli and Dr Grundy are cut form the same cloth......Know their context before you listen to what their opinion of what the data really said. GO back and read the Framingham data sometime.

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 12, 2011
at 01:35 AM

Dr. Castelli clearly agrees that HDL is the best predictor of CVD risk. However, he does not agree that the particle size adds little information. Specifically, LDL size can be discerned based on triglyceride levels, at least according to the Framingham study. Read the transcript where he specifically quotes 99% probability / confidence. His main ponit is that the particle size just lowers the risk vis-a-vis Type B; it is not indifferent to overall CVD risk.

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7 Answers

5
Be1dbd31e4a3fccd4394494aa5db256d

(17969)

on July 12, 2011
at 04:21 AM

I'll try to give my take on it and people can challenge me if they wish, I'm not an expert, I just want to argue.

This is a very good study and free to access. http://atvb.ahajournals.org/content/25/3/553.long

Basically it is looking at the data for LDL subfractions and IHD. The abstract results are:

"Cholesterol levels in the large and small LDL subfractions (termed LDL-C???260?? and LDL-C<255??, respectively) were estimated from polyacrylamide gradient gel electrophoresis of whole plasma in the cohort of 2072 men of the population-based Qu??bec Cardiovascular Study. All men were free of IHD at the baseline examination and followed-up for a period of 13 years, during which 262 first IHD events (coronary death, nonfatal myocardial infarction, and unstable angina pectoris) were recorded. Our study confirmed the strong and independent association between LDL-C<255?? levels as a proxy of the small dense LDL phenotype and the risk of IHD in men, particularly over the first 7 years of follow-up. However, elevated LDL-C???260?? levels (third versus first tertile) were not associated with an increased risk of IHD over the 13-year follow-up (RR=0.76; P=0.07). "

Aha! Do you see that? I mean next to the part about large LDL not being associated with heart disease and small LDL being associated. It says that people with LDL over 260, that big ol' honking group of diabetic obese people who guzzle soda and eat at Mcdonalds, invariably have small dense LDL, very high LDL means an atherogenic profile. If you pool all of the cholesterol data from everyone and these people with massive LDL, most of it small LDL, you will probably find a correlation between non-HDL and heart disease, because the people at the upper end of non-HDL all have an atherogenic profile with small LDL, they inflate the ostensible badness of LDL with their massive LDL and high risk. There are probably some exceptions, it can be genetic + lots of butter, but if it is pattern A we can't extrapolate.

I know that any LDL is potentially atherogenic. Potentially. I wish people wouldn't keep repeating that any LDL is potentially atherogenic as if it is saying something, it is a distraction from the real issue. It is like saying any man is potentially a murderer. What good is that? If we say that all men are potentially murderers, rightfully so, and we point to a lot men together, let's say a football game, can we necessarily expect a murder to happen? It happens, but most of the time it doesn't, so this argument makes no sense. Dr. K over there probably says the word "context" more than anyone else around here, isn't he right? If all LDL is necessarily bad, then how come there is no evidence for inherent badness, only correlations which I have explained above. Just because an LDL particle can become atherogenic doesn't mean that it necessarily will cause heart disease. You are going to have people with a lot of LDL where it is going to turn into atherosclerotic plaque, even pattern A LDL if the biological situation is right, plenty of arterial injury, plenty of oxidative stress and all of those signatures of metabolic syndrome. I think that inflammation is a big player in the progression of atherosclerosis, can we really say that paleos with rock-bottom inflammatory markers are at risk of atherosclerosis? Lookey, the AHA agrees with me, read the whole thing, or even just the conclusion. http://circ.ahajournals.org/content/105/9/1135.full

Paul Jaminet covered what he believes to be a cause of higher cholesterol in paleo diets, low copper http://perfecthealthdiet.com/?p=2547 . What exactly do these CW guys expect people to do about higher LDL? But in actual fact the meta-issue is arterial damage. Are your arteries damaged? You need LDL to carry cholesterol to repair them. Gee I wonder if massive LDL is itself the problem or it is the body's attempt at a solution? Have they ever suggested copper? If they haven't, I don't see a point in listening to them. If they have well then hallelujah we're probably saved.

Also I don't think most of us have LDL over 260, it is just that doctors threaten statins for people with 150 so we try to explain that it's no big deal if their other markers are good. Everyone should be trying to be as healthy as possible in every aspect of micronutrition and the important blood markers, if they are and they have a big scary LDL of 150 and triglycerides of 60, then is that threat of statins valid? Is the panic at any level of LDL higher than necessary to prevent Alzheimer's valid?

I want to be clear that I am not encouraging a laissez faire attitude towards LDL cholesterol so long as trigs, HDL and CRP are good, like I pointed out, it could mean low copper and people should look into it, but in general we have bigger fish to fry.

Be1dbd31e4a3fccd4394494aa5db256d

(17969)

on July 12, 2011
at 04:54 AM

Ah right, maybe I'll steam my fish and cover them with spices.

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 12, 2011
at 06:37 AM

Jack, HDL is your Roto Rooter and way more important than your LDL level or particle size. Get that high if you can. If you can't, check your ApoE status and see if you might be more compatible with a high- or low-fat diet.

Af1d286f0fd5c3949f59b4edf4d892f5

(18472)

on July 12, 2011
at 06:29 AM

some interesting points stabby. in Oct 2010, I had low CRP with similar numbers, so it would seem that inflammation is not an issue for me.but then again, my HDL is super low for the amount of eggs and coconut oil and butter i eat. most paleo folk with so called 'high LDL' also sport a more impressive HDL figure of 60-100 or so. what's a brother gotta do to raise his HDL? drink coconut oil like a cocktail?

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 12, 2011
at 06:18 AM

Castelli actually cites this study: Lamarche, not Lamarck. Those with elevated type A LDL have twice the risk as those with nonelevated type A LDL. If you go to Discussion, it says that those w/high type A LDL levels also have high overall LDL and ApoB, which promote atherosclerosis over a longer term. 260A is not LDL level but the particle size in Angstrom, a nanodistance.

Be1dbd31e4a3fccd4394494aa5db256d

(17969)

on July 12, 2011
at 03:20 PM

To simplify, you say "have high overall LDL and ApoB, which promote atherosclerosis over a longer term" do they themselves inherently promote atherosclerosis or is it that in general in a population that tends to eat a bad diet you will find an association between these things in a population? This is the correlation=causation fallacy and it is an incorrect extrapolation.

44348571d9bc70c02ac2975cc500f154

(5853)

on July 12, 2011
at 10:01 AM

I keep my arteries happy with daily serving of good fish, better than beef me thinks :) HDL is now over 105, but my tc is too high i think, something must be wrong. Its like 460. I would like to see it somewhere around 250

Be1dbd31e4a3fccd4394494aa5db256d

(17969)

on July 12, 2011
at 03:14 PM

Ok Namby I see your point, and I am saying that any associated between "elevated" LDL is probably indicative of the metabolic syndrome and arterial damage, so it makes no sense to extrapolate to paleos with LDL of 150 and say they need to get it to 100, which is essential the relevant conversation here.

Be1dbd31e4a3fccd4394494aa5db256d

(17969)

on July 12, 2011
at 03:28 PM

So basically I'm saying that just because you can find a correlation between elevated LDL and heart disease in a population, that doesn't mean that all increases in LDL are bad in all cases. LDL that is indicative of arterial damage is not the same as LDL indicative of someone with the phenotype that produces higher LDL from eating a lot of butter.

Be1dbd31e4a3fccd4394494aa5db256d

(17969)

on July 12, 2011
at 03:16 PM

Ok Namby I see your point, and I am saying that any associated between "elevated" LDL is probably caused by the cases with the metabolic syndrome and arterial damage, so it makes no sense to extrapolate to paleos with LDL of 150 and say they need to get it to 100, which is essential the relevant. There are big differences between people around here. In a normal population you don't have people eating in such a way to try to elevate their LDL with coconut oil and butter and such, that is completely different from those with lots of arterial damage, and so we shouldn't compare them

21fd060d0796fdb8a4a990441e08eae7

(24543)

on July 12, 2011
at 04:49 AM

Do you mean to say that we have bigger fish to poach? Because frying a big fish could be bad for your cholesterol. And big fish have more mercury than small fish. Other than that, all good points. Except that associations in cohort data are still quite susceptible to misinterpretation due to confounders. I must admit though, my attitude towards studies is way more laissez faire when the condition being studied doesn't apply to me. If I had super high cholesterol, my views might be very different.

Be1dbd31e4a3fccd4394494aa5db256d

(17969)

on July 12, 2011
at 03:15 PM

Ok Namby I see your point, and I am saying that any associated between "elevated" LDL is probably indicative of the metabolic syndrome and arterial damage, so it makes no sense to extrapolate to paleos with LDL of 150 and say they need to get it to 100, which is essential the relevant. There are big differences between people around here. In a normal population you don't have people eating in such a way to try to elevate their LDL with coconut oil and butter and such, that is completely different from those with lots of arterial damage, and so we shouldn't compare them.

Be1dbd31e4a3fccd4394494aa5db256d

(17969)

on July 12, 2011
at 03:17 PM

Ok Namby I see your point, and I am saying that any associated between "elevated" LDL is probably caused by the cases with the metabolic syndrome and arterial damage, so it makes no sense to extrapolate to paleos with LDL of 150 and say they need to get it to 100, which is the discussion. There are big differences between people around here. In a normal population you don't have people eating in such a way to try to elevate their LDL with coconut oil and butter and such, that is completely different from those with lots of arterial damage, and so we shouldn't compare them.

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 13, 2011
at 05:04 AM

Stabby, PHD cited deficiencies in copper, choline and even iodine as possibly causing arterial damage, which would then increase LDL. That seems plausible among Paleos who've changed their diets but the above Quebec study involved a whole cross section of male population, some of whom would suffer from familial cholesterolimia. For them, if you eat fat, your chol would go up. (Whether they should be on a low fat diet is another question; I'm not sure).

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 12, 2011
at 06:22 AM

Even though the conclusion is made regarding association, the benchmark is "increased risk from teh baseline". There is relative risk with elevation in type A LDL level. In other words, MORE of A is BAD. I think that's exactly what Castelli is saying.

Be1dbd31e4a3fccd4394494aa5db256d

(17969)

on July 13, 2011
at 06:29 PM

There will be a way to figure out. Give it some time at low inflammation, good antioxidant status, and high fat, and then check the amount of oxLDL. I'm not convinced that lots of LDL necessarily means lots of oxLDL. Although in people eating normal diets it might look like that, so I think I know where some people are coming from, I just don't agree that it applies to all situations.

Be1dbd31e4a3fccd4394494aa5db256d

(17969)

on July 13, 2011
at 05:45 AM

What you suggested is also possible. Whether or not those people would necessarily be better off with lower LDL is hard to say. Kurt Harris had a post a while ago questioning whether or not these people actually needed to try to lower their levels if their inflammation was low and their arteries were healthy. I don't know about that one, but I'll certainly consider it.

Be1dbd31e4a3fccd4394494aa5db256d

(17969)

on July 13, 2011
at 05:44 AM

It isn't just nutrient deficiencies but anything that damages the arteries. It is very plausible that we have a large percentage of the population with severely damaged arteries. Dietary changes to include more coconut and butter will increase cholesterol levels if there is a need for cholesterol. Someone starting a paleo diet with damaged arteries from deficiencies and everything else that damaged them would need a lot of cholesterol. If they failed to increase levels of those nutrients or resolve all of their inflammation then their levels would remind elevated.

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 13, 2011
at 05:07 AM

But even Dr. Lustig attested to this. See my prior post regarding ApoE. For 25% of the population, high fat leads to high cholesterol. Doesn't this seem a bit more plausible: that the 1/4 of the population just don't do well on a high fat diet because of they're type 4s? And we have lots of them! Than that we have a mass epidemic of Cu, I, and choline deficiency affecting the general population? Paul's point seems sound and reasonable but I'm not so sure at the population level whether the deficiency is due to an abrupt dietary change (as it seems to have been for Larry, according to Paul).

Af1d286f0fd5c3949f59b4edf4d892f5

(18472)

on July 13, 2011
at 06:00 PM

This is a good discussion guys. Because even if I test for ApoE, and find that I am type 4, which means eating fat increases LDL for me, I wouldn't want to jump to the conclusion that naturally having a higher LDL is 'bad'. What if it's more true to say that's it's 'necessary' for me to have the higher LDL transports if I choose to eat a higher amount of fat. Most other Paleos I've seen are also able to get their HDL up prety high too though. To me, if I had a very robust HDL, I probably wouldn't feel like I had much to be concerned about.

5
D1c02d4fc5125a670cf419dbb3e18ba7

on July 12, 2011
at 01:26 AM

Chris Masterjohn via Melissa just responded to Jack Kronk's VAP post that somewhat addresses your question. http://paleohacks.com/questions/50347/hack-jack-kronks-vap-test-results#axzz1RqfiQNjS

Here is the relevant excerpt -

Studies of cardiovascular mortality suggest that among all of these measures, total-to-HDL-C ratio is the strongest predictor and neither adding triglycerides nor LDL particle size adds any additional information....

There is an additional reason I'm skeptical of giving preference to particle size. There is, as yet, no standardized way to assess it, and the different methods are in wild conflict with each other. In one study, they sent 40 samples to labs using four different methods of analysis, and all methods agreed on the classification only 8% of the time. Tube gel electrophoresis identified about 80% of people as type A whereas VAP identified 8% of people as type A. You can increase your particle size even more, according to a different study, by having it analyzed by HPLC.

21fd060d0796fdb8a4a990441e08eae7

(24543)

on July 12, 2011
at 04:40 AM

N. Pamby-- the Cordain bit was just an analogy :)

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 12, 2011
at 04:01 AM

Kamal, correct, the 99% confidence Castelli cites is from the Berkeley study, not the Framingham study. But he readily admits that he missed the importance of triglycerides early and kicks himself for it. What the Framingham study found is the additional correlation between the number of LDL particles (not particle type and not LDL level) and triglycerides. The higher # of LDL particles ==> high triglycerides. What is indisputable is the importance of HDL: i.e., Total Cholesterol / HDL < 3.5 if you can help it. This is not what many (incl. Castelli) expected. Yet they had to embrace this.

Ed71ab1c75c6a9bd217a599db0a3e117

(25472)

on July 12, 2011
at 02:26 AM

Dr Castelli and Dr Grundy are cut form the same cloth......Know their context before you listen to what their opinion of what the data really said. GO back and read the Framingham data sometime.

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 12, 2011
at 01:35 AM

Dr. Castelli clearly agrees that HDL is the best predictor of CVD risk. However, he does not agree that the particle size adds little information. Specifically, LDL size can be discerned based on triglyceride levels, at least according to the Framingham study. Read the transcript where he specifically quotes 99% probability / confidence. His main ponit is that the particle size just lowers the risk vis-a-vis Type B; it is not indifferent to overall CVD risk.

21fd060d0796fdb8a4a990441e08eae7

(24543)

on July 12, 2011
at 02:56 AM

Believe it or not, people can say different things at different times. Not everything a Framingham author says for perpetuity is based on Framingham study data. In fact, almost nothing Dr. Castelli says above is based on Framingham. It's like if I saw a posting about Loren Cordain and said "Don't believe anything he says about indigenous diets...his view on saturated fat was wrong."

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 12, 2011
at 04:06 AM

W/regard to Cordain, I don't think he really changed his position and you can't say his SFA position is "wrong". He said that SFA causes plaques. The current debate is no longer the existence of plaques but what will instigate a cardiac event: i.e., inflammation. But is SFA atherogenic? I think so, even those Inuits have plaques, according to Cordain.

2
Ed71ab1c75c6a9bd217a599db0a3e117

(25472)

on July 12, 2011
at 02:22 AM

Dr Castelli should re read Framingham data, because his perception is not what is published.

Framingham data was REPORTED to say that heart disease correlated with heart disease best. At specific times the researchers released information from the trial based upon their interpretations. At 16 years in those who developed heart disease only showed an 11% increase in serum cholesterol levels. Yet researchers used the words, ???striking increase??? to describe the effect. In 1987 the 30 year data was released on cardiovascular disease and this time they told us that CardioVascular mortality correlated with higher cholesterol in patients below 50 years old, but after this age they reported NO RELATIONSHIP with cholesterol and CV mortality. Stop and think about that. Do patients get treated this way today? Why is everyone placed upon a statin you may ask for a cholesterol over 200?

For those aged over 50 with a decreasing level of cholesterol as they age they actually had an increase in CV mortality and all causes of mortality in the entire study! So if you are over 50 and your cholesterol is lowered (statin anyone) Framingham says you will die sooner from all causes!

Read this quote from the update, ???There is a direct association between falling cholesterol over the first 14 years and MORTALITY over the following 18 years?????? WOW! The data showed that for every 1 mg/dl drop in cholesterol per year, there was a 14% increase in the rise of overall mortality.

So I completely accept that doing studies like Framingham are great for us as a nation to gain insight into trends on health and disease. But the real problem with relying on this data is really understanding what the trials really found. You can???t leave the interpretation of the data up to groups who have a vested or financial interest in the outcome. Dr. Grundy, the lead investigator in the trial, was found to make millions off his opinions of what Framingham said to him and his friends in the pharmaceutical industry. He also controlled what got published in the journal, Circulation, at this time. How convienient!

www.ncbi.nlm.nih.gov/pubmed/3560398

http://content.onlinejacc.org/cgi/content/full/33/5/1136

21fd060d0796fdb8a4a990441e08eae7

(24543)

on July 12, 2011
at 02:58 AM

Yes. Framingham is way misleading, obviously. But what specifically does this have to do with LDL particle size?

Ed71ab1c75c6a9bd217a599db0a3e117

(25472)

on July 13, 2011
at 01:10 AM

The opinions from Framingham of why we have statin nation what Framingham really found was not important to the opinion makers in big pharma's pocket.

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 13, 2011
at 12:41 AM

There is so much noise floating around and it's hard to discern who's telling the truth. This is why you have to actually read the articles yourself, to see who's really telling the truth. I only have access to the abstract for the first link. The second article seems open and reasonable: I don't really see any bias in interpreting what the study found.

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 13, 2011
at 01:11 AM

So LDL is not THE factor, that's obvious and no one, not the Farmingham authors, is disputing that. The strongest factor is age, since it's no brainer. All people die. In the U.S. around the 80s, most people died from 2 things: CVD or cancer. If you died from cancer, does that imply you didn't have CVD? No, cancer just killed you off sooner. There is a limitation in interpretation and I think some of you are making wild inferences without reading the text.

21fd060d0796fdb8a4a990441e08eae7

(24543)

on July 13, 2011
at 02:55 AM

What is at fault is the discussion sections of papers stemming from Framingham, not the data in and of itself. There are like a billion of these papers in various journals, so you can't generalize, as well as dozens of authors. But by large, they fall into the same trap that biostatisticians figured out decades ago: correlation does not mean causation, and cohort studies are meant to be hypothesis generating and not the backbone of a national agenda. I can't fault them too much for it--very few academic researchers are actually evil. The professors at my school fully believe what they say.

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 13, 2011
at 01:17 AM

Dr. K, I think you're talking about the opportunists and the pharma industry. Sure, there are MDs in the medical-pharma complex. But I don't see evidence of Castelli and Levy overstating what they found, based on just the article read. Grundy, I do not know but those who conducted the study seem to be more or less reasonable.

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 13, 2011
at 12:39 AM

No, Kamal, it seems that Dr. K is saying that those who interpreted the Framingham study did so misleadingly. The study itself does not seem to be misleading. They freely admit what they found -- what was statistically significant or not.

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 13, 2011
at 01:08 AM

The authors point out that these variables are overlapping, which could be misleading when trated separately. Obesity is related to lack of exercise, which is related to onset of diabetes which is related to age. As separate variables their significance is somewhat understated than whey they're seen as a whole, which contribute to the overall CVD risk. In other words, you might not get significant relatioship in LDL with CVD if you don't smoke, are not obese, are not diabetic, have high HDL, are not of certain age, etc. But if some of these are true, it may be another story.

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 13, 2011
at 12:52 AM

Based on the 2nd article, the authors (Castelli, Levy and Anderson) freely admit that heart disease is a "multifactorial disorder" -- no independent variable captures strong association other than age, smoking or not, and HDL. But as a whole, when you pile these things up, they amount to strong correlation. This is just a review article; no separate analysis is presented and no conclusion is drawn other than the obvious: CVD has many variables, not one smoking gun but many smoking guns which, in totality, add up. Like life, CVD is complex. What else did the authors say?

Ed71ab1c75c6a9bd217a599db0a3e117

(25472)

on September 05, 2011
at 02:26 AM

Lol at those last two statements. I completely believe the opposite

2
6120c989fd5b69f42a0834b69b87955b

(24553)

on July 12, 2011
at 02:14 AM

Isn't the real thing we should be worrying about is having nice slippery and shiny arterial walls, so that the cholesterol doesn't having to go around patching things up? I'm starting to think that blaming cholesterol plaques for heart disease is along the lines of blaming paramedics for the injuries arising from car crashes.

Now the question is, how do we keep our arterial walls nice and happy? Getting enough saturated fat? Magnesium? Better Omega 3-6 ratios? Reduced stress?

3c6b4eed18dc57f746755b698426e7c8

(5152)

on July 12, 2011
at 09:47 PM

If you want your arteries totally shiny and slippery, no plaques, you have to practice veganism! At least that's what the vegans say. If you are a vegan and your cholesterol is below 150, you have no plaque. Again, I'm quoting Dr. Castelli and some vegans. I do not know if that's true.

6120c989fd5b69f42a0834b69b87955b

(24553)

on July 13, 2011
at 01:16 AM

I went and did more reading, and it looks like I had been oversimplistic in my own understanding of how plaque builds up. Apparently, the endothelium is more like a window screen than a stainless steel countertop, and plaque also builds up behind it. Wouldn't all the PUFA in a vegan diet oxidize and cause more problems. I definitely welcome anyone with more understanding of this to chime in here, I'm still learning.

0
Bb4e38b52b0743e5cc3f8975c3ab1561

on February 15, 2012
at 07:50 PM

The correlations are not perfect and some numbers may be misleading.

First, if you have low TG's, since most values of LDL are calculated using a TG/5 subtraction, if you have low TG's your LDL number will look elevated. There is an alternate Iranian version used which gives lower numbers for LDL if your TG's are below 80 or so (as mine are).

Second, I have a family history with almost no heart disease. My grandpa will turn 101 this June and my grandma on the OTHER side of the family lived to be 98. Of course I hope I take after them. My HDL has been between 32 to 40 for the last 15 years, usually between 35-38.

I am moderately active and dance a few times a week. I do take fish oil but my TG's were often low even before I started this. My total cholesterol has varied between 160-230 the last 20 years, usually in the 180-190 range with a few in the 200-219 range the last 15 years.

But I think I read above that there is a correlation of high TG's with low HDL. I have both low HDL and low TG's. Supposedly there are really 12 different kinds of HDL but I don't know how that relates to health and if that could explain my low HDL.

The ratio of TG/HDL should be low to have the large, fluffy type A LDL (below 2.0 is very good) and since both my TG and HDL are low, I do fall into this category.

Time will tell I guess.

0
928331b87bfa52da4c521d73ef79927b

on September 04, 2011
at 05:31 PM

It's been proven that a low fat, plant based diet will not only prevent but reverse heart disease. Eliminate processsed oils and all other processed foods and stick to a whole foods / plant based diet and you'll cut your chances of cardiac events to slim to none.

Dr. Caldwell Esselstyn took 18 of the sickest heart patients, put them on a plant based diet without processed oils and not only stopped their disease but reversed it in most cases.

You comment about starch and Triglycerides couldn't be further from the truth. I went totally plant based and only eat carbs and starches in my diet. My Tri's fell from 275 to 50 within 6 weeks. Dr. John McDougall has proven time and time again that a low fat, starch diet is not only healthy for a person but eliminates disease.

I was a total skeptic until I did my own experiment on myself. I eliminated animal products one by one and tested via Berkeley Heart Lab along the way. As each animal product went away my numbers continued to follow suit and fall. After 3 months my total was below 150 from 220 and Tri's went from 275 to 50. My HDL increased and LDL fell. My LDL particle size also slightly increased.. But mine is very large at 273 on the Berkeley scale. My HDL's are in the mid range.

I am yet to see any studies that support consuming animal products to stop / reverse heart disease. Believe me, if the data was there I'd be enjoying hamburgers and cheese pizza.

But for now I'll stick to my plant based diet..... The quality of how I feel totally outweighs the pleasure of eating standard American food.

Bcad307b240275ae3f5820ba6eb4a712

(923)

on September 04, 2011
at 07:07 PM

What do your strawmen about hamburgers, cheeese pizzas, and standard American food have to do with paleo dietary philosophy?

Ed71ab1c75c6a9bd217a599db0a3e117

(25472)

on September 05, 2011
at 02:29 AM

Dr. Caldwell Esselstyn is at the Cleveland clinic, a retired general surgeon with zero nutrition training but huge ties to the vegan community and their agenda. Major fucking pass from me. This guy is going to kill many people. Him and ornish are in bed together. Once jobs and clinton die we will see how this goes.

3c6b4eed18dc57f746755b698426e7c8

(5152)

on March 20, 2012
at 06:21 AM

I have a little different take on this. I've gone on a 60% carb diet, after having done 20% carb, 60% fat and 20% prot. My TC did fall from 225 to 160; so that part is true ... however, my TG did increase to 115 from 90. The part that fell was the LDL: from 110 to 80. I definitely think that in some subgroup (possibly ApoE4 or ApoE2), LDL WILL fall by consuming more whole food carbs and cutting fat.

0
36d4865f591d55c9eff666fd82ab8ada

on July 12, 2011
at 03:11 AM

Does anyone have any information about whether it is just the oxidized LDL that causes the damage. I have read that cigarette smoking, lack of exercise, and/or systemic inflammation can all cause LDL to oxidize, and that's what causes arterial plaque buildup. Therefore, a high LDL level alone, supposedly, should not cause plaque buildup unless the LDL is being oxidized. Can anyone comment on that? Thank you.

D1c02d4fc5125a670cf419dbb3e18ba7

on July 12, 2011
at 03:06 PM

You might want to look at Chris Masterjohn's blog (The Daily Lipid) since I believe he has written about this. Also check out this podcast with him. In the comments section, there is some discussion about oxLDL also - http://thehealthyskeptic.org/the-healthy-skeptic-podcast-episode-11 Finally, here are some links from Stephan Guyenet- http://wholehealthsource.blogspot.com/2009/07/diet-heart-hypothesis-oxidized-ldl-part.html http://wholehealthsource.blogspot.com/2009/08/diet-heart-hypothesis-oxidized-ldl-part.html

928331b87bfa52da4c521d73ef79927b

(40)

on September 04, 2011
at 05:34 PM

Are you kidding me? Chris is not even a doctor! Why someone would even waste their time listening or reading something from this person is beyond me! You have countless of established / trained medical professionals that have peer reviewed studies released. And you want to put your life in the hands of some layman?

B2f2d854c1f60630089ba6f413618868

(0)

on May 26, 2012
at 10:17 PM

Chris is far from a layman. He is a PhD candidate in nutritional sciences with a concentration in biochemical and molecular nutrition. He has two peer reviewed papers that can be found on pub med.

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