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:
and heard here:
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?
asked byNamby_Pamby (5152)
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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.
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.
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!
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?
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.
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.
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.