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Dean Pomerleau

Beyond LDL - Is Cholesterol Particle Size Worth Testing?

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All,

 

We had a pretty long thread not too long ago about Total Cholesterol and Heart Attack Risk but as far as I can tell we haven't talked much about the relative value of a standard lipid panel vs. some of the newer tests for various LDL particle sizes, densities etc. 

 

I bring it up for two reasons:

 

One is personal. A  family member in their early 50s is an APOE4 carrier (single allele) and not surprisingly, has borderline high cholesterol (210 mg/dL total, 120 LDL, 55 HDL). They are otherwise thin, active, healthy with good fasting blood glucose. So it seems they are one of those borderline cases for statins, and I'm wondering whether getting their LDL particle sizes tested might provide some additional useful diagnostic information for making that decision. I would lean against starting statins in their case (due to possible side effects see below), but I'm wondering if the discovery that they have many (or very few) small dense LDL particles might tip the scales one way or the other.

 

The second reason I bring it up is because I just listened to a long (1:20:00) but very interesting interview by Dr. Rhonda Patrick with Dr. Ronald Krauss, who appears to be a pioneer in research into cholesterol and CVD, the effects of diet on CVD risk, statin side effects, particle size testing etc.

 

I found it really educational to learn more about the mechanics of atherosclerosis, e.g. the details of how inflammation is involved and why we might have evolved to work that way. How small LDL particles have the part of their surface structure occluded just where the liver's LDL-receptor tries to attach to them, making the small particles harder to clear from the bloodstream, making them stick around in the bloodstream for longer to get oxidized / glycated and to infiltrate the arterial walls. Lots of good stuff I didn't know before.

 

But a couple caveats. I'm not an expert on the details of how atherosclerosis works, or anything about particle sizes, so while I found it interesting, I can't vouch for the validity of Dr. Krauss's perspective or the information he shared.

 

And I will note that Dr. Krauss co-authored with Dr. Patty Siri-Tarino and several others a pretty poor and misleading meta-analysis which appeared to call into question the link between saturated fat and heart disease. Their meta-analysis has been roundly criticized briefly by Michael in this thread and more thoroughly by PlantPositive here

 

He also mentioned he's been sponsored by the dairy industry, and has a patent and receives royalties on a new cutting edge LDL particle measurement test called Cardio IQ® Lipoprotein Fractionation, Ion Mobility which is now available from Quest. 

 

So all that is to meant to suggest that one should take what Dr. Krauss says in this interview with a pretty grain of salt. I'd be curious to hear what anyone with more knowledge in the area has to say about particle size testing, as well as the information Dr. Krauss shares both about the etiology of atherosclerosis and the significance of "small dense" LDL particle count vs the standard LDL measure on a lipid panel, particularly for people with borderline risk of CVD.

 

To his credit, Dr. Krauss acknowledges that particle testing isn't for everyone. People at either extreme (i.e. very low or very high LDL cholesterol) probably don't need it - for obvious and opposite reasons.

 

It's only in the borderline cases, like my family member, where it might be helpful. He also said the standard heart attack risk calculators, which don't take into account anything about particle size, do a pretty good job, and particle size and counts doesn't add very much to their accuracy / predictive power. But he sticks by idea that mechanistically, it's the small dense LDL particles that matter most for CVD risk. He also talks about how statins do work, but don't work as well as you might think because they upregulate the liver's LDL-receptor, which is pretty ineffective at clearly the most atherogenic particles - the small dense ones.

 

He talks about statin side effects (muscle pain / weakness, but especially increased risk of diabetes, particularly in women). He is very much in favor of diet and lifestyle interventions to manage CVD risk, but as a researcher and clinician, he says there is trouble both proving the benefits of diet/lifestyle on CVD risk in clinical trials, and convincing his patients to adopt diet and lifestyle modifications, due both to compliance issues, and also in terms of getting the funding to do the research to make a convincing case. He says it's much easier to both get funding for, and to conduct, research on statins and other pharmacological interventions, because there is money to be made, and compliance is much less of an issue. 

 

Whether or not Dr. Krauss is blowing smoke about the value of particle size testing, it seemed to my (admittedly relatively naive) ears that Rhonda had a good set of questions and Dr. Krauss had clear and well thought out set of answers. For anyone interested in the topic, check out the show notes below and give it a watch/listen and let us know what you think.

 

--Dean

 

 

Begin Show Notes
==============
Dr. Ronald Krauss on LDL Cholesterol, Particle Size, Heart Disease & Atherogenic Dyslipidemia 

In this podcast, I interview my friend and colleague Dr. Ronald Krauss.

Ronald Krauss, M.D. is the director of atherosclerosis research at Children’s Hospital Oakland Research Institute, Adjunct Professor at UCSF and UC Berkeley. Dr. Krauss is really one of the pioneering scientists that changed the way we all think about cholesterol and saturated fat. The work of Dr. Krauss has demonstrated that smaller, denser LDL particles, which he pioneered a test for, known as the "Ion Mobility" test, has special significance when it comes to determining risk of heart disease. Regrettably, this test is not yet universally employed in a clinical setting in the manner in which total LDL cholesterol is, however. This test is called Cardio IQ® Lipoprotein Fractionation, Ion Mobility and is offered by quest diagnostics.

 

Dr. Krauss is responsible for having played a part in the actual guidelines used by the American Heart Association in his role as chairman of the Nutrition Committee. Additionally, Dr. Krauss has also served on both the Committee on Dietary Recommended Intakes for Macronutrients and the Committee on Biomarkers of Chronic Disease of the Institute of Medicine of the National Academy of Sciences.
 

In this podcast, Ron and I discuss what HDL and LDL cholesterol are, what they do in the body and how they play a role in heart disease. We talk about what small, dense LDL particles are, how they form, what effect eating saturated fat versus refined carbohydrates have on LDL particle size and heart disease risk and more generally what the main risk factors for heart disease are. Ron also talks about the good, bad and the ugly of LDL-lowering drugs known as statins and much more.

 

 
 
In this conversation, Ron and I discuss...
  • Changes in the availability of funding for good nutritional research.
    • "It's a fact that NIH, which is the major funder of biomedical research in the world, has basically pulled the plug on clinical research support as a general area of emphasis. The infrastructure for doing good nutritional studies, in particular, has relied on a mechanism that is now being withdrawn." - Dr. Ronald M Krauss
  • The important difference between consumption of dietary cholesterol, which has a negligible influence on heart disease risk, and cholesterol produced endogenously in the body (which can be a marker of risk, depending on a complete profile).
  • The good, bad and the ugly of LDL-lowering drugs known as statins and much more. 
  • What differentiates fructose from fruit versus fructose as an added sugar, namely: speed of absorption, presence or absence of other beneficial compounds (fiber, micronutrients, polyphenols, etc.), and differences in dose.
  • How LDL (low-density lipoprotein), and particularly the ApoB protein inside of LDL, is needed to transport cholesterol, triglycerides, and fatty acids throughout the bloodstream in order to deliver them to other tissues in the body that may need them. 
  • What small, dense LDL particles are, how they form, what effect eating saturated fat versus refined carbohydrates have on LDL particle size and heart disease risk and more generally what the main risk factors for heart disease are.
  • The functional difference between large, buoyant LDL particles and small, dense LDL particles and introduces us to the traits of what he terms "atherogenic dyslipidemia." These traits consist of:
    1. High levels of small, dense LDL cholesterol. 
    2. Low levels of HDL cholesterol. 
    3. High levels of triglyceride-rich lipoproteins (very-low-density lipoproteins or "VLDL") and their remnants.
       
  • How small, dense LDL particles increase the risk of atherosclerosis. There is only one ApoB protein per LDL particle, which is what enables ApoB to be a surrogate blood biomarker for LDL particle number.
  • How access to the ApoB protein can become obscured due to conformation changes in the small, dense LDL particles. As the size of the particle decreases, this conformation change reduces the ability for the particle to bind to the LDL receptor and be recycled by the liver.
  • How VLDL particles, the precursor to LDL, demonstrate an interaction with LPS (also known as endotoxin, a component of bacterial cell membranes), and how it's possible that some of the negative associations with this particle size may be a result of their simply being in the blood stream longer: this gives them a greater opportunity to undergo inflammatory transformations.
    • This part is especially exciting to me because it may be an interesting link by which gut health (where much of the bacteria and immune cells in the body are located) and the importance of controlling inflammation to cardiovascular health.
  • How saturated fat appears to increase the larger, more buoyant LDL particles, which do not have the same robust correlation to heart disease risk that the smaller, more dense particles do. Dr. Krauss also takes the stance that consumption of saturated fat does not have as strong of a link to heart disease risk as previously suggested by others, and may be less relevant except in the case of what he termed "hyper-responders." These "hyper-responders" have gene polymorphisms that cause them to respond differently to saturated fat.
  • How increased carbohydrate consumption, especially simple sugars may have been an unintended consequence of the push for low-fat diets, and how this increased traits associated with atherogenic dyslipidemia: namely, a shift from the larger, more buoyant LDL particles to the smaller, more dense LDL particles.
  • Broadly, the differences between the various types of lipoprotein particles, including very-low-density lipoproteins (VLDL), and high-density lipoprotein (HDL) and what their roles are in the body.
This really is one of the better science-based podcasts I've posted to date. It's often a bit nuanced, but hopefully with the help of some of the annotations in the video you will find it as enriching as I have. Dr. Krauss is a real pioneer in the field and drops huge amounts of knowledge, so go check it out now!
 
==============
End Show Notes

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(Psst: Dean, images as https, please!)
 

But a couple caveats. I'm not an expert on the details of how atherosclerosis works, or anything about particle sizes, so while I found it interesting, I can't vouch for the validity of Dr. Krauss's perspective or the information he shared.


Well, that's presumably why you posted ;) .
 

And I will note that Dr. Krauss co-authored with Dr. Patty Siri-Tarino and several others a pretty poor and misleading meta-analysis which appeared to call into question the link between saturated fat and heart disease. Their meta-analysis has been roundly criticized briefly by Michael in this thread and more thoroughly by PlantPositive here.


FWIW, I think that while the Siri-Tarino meta-analysis is misleading in practice, they are neither stupid (as Chowdhury et al, and de Sousa et al seem to be) nor ill-motivated, and the while a lot of Atkins extremists seized upon it as evidence completely exculpating SaFA, the authors themselves cautioned (albeit initially buried in the original report) that they were only looking at total intake and not at substitution effects, and made this the major subject of a subsequent paper.(1)

That said, while Krauss has done a lot of pioineering work on lipidology and his early work on particle size did look very promising and mechanistically appealing, I'm surprised to learn that Krauss is still supporting LDL particle size, as the issue is scientifically dead in the water as far as I can see.
 

Dr. Krauss is responsible for having played a part in the actual guidelines used by the American Heart Association in his role as chairman of the Nutrition Committee. Additionally, Dr. Krauss has also served on both the Committee on Dietary Recommended Intakes for Macronutrients and the Committee on Biomarkers of Chronic Disease of the Institute of Medicine of the National Academy of Sciences.


You will note, however, that the AHA has not adopted LDL size testing for determination of residual risk, and neither has any other major scientific organization. There's a reason for that. The real issue, as we've seen in subsequent years (and kinda knew in the first place from theory), is the number of atherogenic (apolipoprotein B (apoB)-containing) lipoprotein particles in circulation (which includes number of LDL particles but also VLDL particles etc), either measured as such or as or numbers of LDL particles per se (LDL-P) measured by nuclear magnetic resonance spectroscopy ("NMR LipoProfile"). Several major scientific organizations have endorsed one or the other or both to assess residual risk.
 
LDL size (either averaged, as earlier studies did, or assessed as numbers of small- vs. large-LDL particles) manages to indirectly capture some of the people with low-to-normal LDL cholesterol who actually have a high particle count, but it's a sloppy surrogate and it generates a misleading understanding of the mechanisms of disease.
 
In particular, (2) was the one study to most clearly resolve the whole LDL-C vs. LDL particle number vs. LDL particle size dynamic. The results are nicely interpreted by the lead author in this article:
 

LDL Particle Size: Does It Matter?
small and large LDL particle concentrations [ie, numbers of each kind of particle] were inversely correlated with each other (Spearman correlation coefficient - 0.64) and they correlated in opposite directions with [average] LDL size. Without accounting for LDL subclass correlation, LDL size and small LDL-p separately were associated with IMT [intima-media thickness, a noninvasive marker for atherosclerosis] (- 20.9 and 31.7 micron change in IMT per 1-SD, respectively, both P < 0.001), but large LDL-p was not (4.9 microns, P = 0.27).

However, after accounting for their inverse correlation, both LDL subclasses [ie, both large and small particles] showed highly significant and independent associations with IMT (36.6 and 52.2 micron higher IMT per 1-SD of large and small LDL-p respectively, both P < 0.001). Interestingly, there was a greater difference in IMT per large LDL particle compared with small LDL when compared on a per particle basis (17.7 and 11.6 microns per 100 nmol/L of large and small LDL-p respectively, both P < 0.001). Smaller LDL size was no longer significant after taking into account the particle concentrations of the two LDL subclasses and risk factors.


Basically, the reason why small LDL particle distribution LOOKS more risky for CVD or events in some studies is that AT A GIVEN LEVEL of LDL-C, smaller particles means more particles — and it's the number of LDL particles (or rather (again), apoB-containing lipoproteins,) that ultimately drives disease, with LDL-C as a marker for LDL-P that works well for most people because the two are closely correlated, but that works poorly for people with extreme size distribution because it skews the normal relationship between LDL-C and particle number.
 
And, the "atherogenic profile" of small, dense LDL typically arises in people eating higher (generally crappy-) carb, low-fat diets, leading to associated low HDL, high TG, and often metabolic syndrome — all of which can be assessed directly without resorting to LDL particle size as a surrogate. Small, dense LDL particles are no more atherogenic than large ones: they are just surrogate markers for discordance between LDL-C and apoB/LDL-P, driven by insulin resistance and other underlying metabolic problems for all of which we have direct assessments.

Here is a pop-press piece on a previous study(3), which uses apoB :
 

ApoB, but not LDL particle size, provides predictive value in assessment of risk

With the LDL-cholesterol/ApoB ratio used as a surrogate for LDL particle size, there was an inverse relationship between the risk of fatal MI and the LDL-cholesterol/ApoB ratio after adjustment for age and gender, indicating that risk increases as LDL size decreases. When adjusted for triglycerides, however, the relationship was no longer statistically significant.


Also note that while it's atherogenic (apoB-containing) lipoproteins that cause disease, not cholesterol per se, high LDL is still plenty predictive: "High plasma LDL was also associated with a twofold greater risk of heart disease after adjustment for lipid and nonlipid risk factors." But particle number reflects the underlying cause, and it captures the (significant) number of people at the extremes of distribution whose LDL-C is misleading.
 
As I mentioned in an earlier discussion with Zeta, a meta-analysis done by the American Association for Clinical Chemistry Lipoprotein and Vascular Diseases Division Working Group on Best Practices on the relative merit of NMR LipoProfile vs. apoB in predicting cardiovascular and other outcomes found them to be roughly equivalent; an article written in response, one of whose two lead authors is a LipoScience employee, could only point at suggestive trends favoring the LipoProfile in a non-systematically selected subset of those studies favoring their test.

At the time of that post, I indicated based on data to hand that if cost were equal I'd go for NMR LipoProfile, but LEF was charging a lot more for NMR LipoProfile than ApoA-1 + apoB + their molar ratio, so the latter seemed more sensible; however, the cost of the former has come down very substantially in ensuing months, which would have swayed me toward LipoProfile.
 
Recently, however, a group including LipoScience employees published a study(4) purporting to show "substantial discordance" between the two, whose results are actually if anything disfavorable to their own test. Not only does it show that the number of people captured as being at higher risk by either test and not by the other is small and about equal for each (and remember, we're talking about a small minority within the minority whose risk isn't captured by regular LDL-C in the first place), but that the reasons that could be assessed directly are more routine and cheaper to test for apoB than for NMR:
 

Similar numbers of patients were identified as at-risk by LDL-PNMR when apoB levels were < 69 mg/dL (5%-6%) and by apoB values when LDL-PNMR was < 1073 nmol/L (6%-7%). Discordance (LDL-PNMR > apoB) was associated with insulin resistance, smaller LDL particle size, increased systemic inflammation, and low circulating levels of “traditional” lipids, whereas discordance (apoB > LDL-PNMR) was associated with larger LDL particle size, and elevated levels of lipoprotein(a) and lipoprotein-associated phospholipase A2 (Lp-PLA2).(4)

 
That is, if test apoB level and the result is misleadingly reassuringly low, the hidden risk will largely be caught if you have measures of insulin resistance and inflammation tested, and it's likely to occur in people whose LDL-C is low to begin with (who aren't really likely in need of specialized testing in the first place), whereas if you go for a LipoProfile and get back a misleadingly low LDL-P, you'd only detect that by testing Lp(a) and Lp-PLA2.
 

The important difference between consumption of dietary cholesterol, which has a negligible influence on heart disease risk, and cholesterol produced endogenously in the body (which can be a marker of risk, depending on a complete profile).


This is true for most people eating omnivorous diets, which contain significant amounts of SaFA and cholesterol, and elevated cholesterol because of overweight and lack of exercise, so the additional effect of an egg or two a day on circulating cholesterol is modest. However, if you have very low intake of these (eg, lacto-ovo vegetarians who don't get much cholesterol otherwise), the additional effect of dietary cholesterol (eg, from whole eggs) can be substantial, especially if you otherwise have a healthy lifestyle. 
 
It's a moot point for vegans, of course.
 
Reference
1: Siri-Tarino PW, Sun Q, Hu FB, Krauss RM. Saturated fatty acids and risk of coronary heart disease: modulation by replacement nutrients. Curr Atheroscler Rep. 2010 Nov;12(6):384-90. doi: 10.1007/s11883-010-0131-6. Review. PubMed PMID: 20711693; PubMed Central PMCID: PMC2943062.

2: Mora S, Szklo M, Otvos JD, Greenland P, Psaty BM, Goff DC Jr, O'Leary DH, Saad MF, Tsai MY, Sharrett AR. LDL particle subclasses, LDL particle size, and carotid atherosclerosis in the Multi-Ethnic Study of Atherosclerosis (MESA). Atherosclerosis. 2007 May;192(1):211-7. PubMed PMID: 16765964.

3: Jungner I, Sniderman AD, Furberg C, Aastveit AH, Holme I, Walldius G. Does low-density lipoprotein size add to atherogenic particle number in predicting the risk of fatal myocardial infarction? Am J Cardiol. 2006 Apr 1;97(7):943-6. Epub 2006 Feb 13. PubMed PMID: 16563891.
 
4: Varvel SA, Dayspring TD, Edmonds Y, Thiselton DL, Ghaedi L, Voros S, McConnell JP, Sasinowski M, Dall T, Warnick GR. Discordance between apolipoprotein B and low-density lipoprotein particle number is associated with insulin resistance in clinical practice. J Clin Lipidol. 2015 Mar-Apr;9(2):247-55. doi: 10.1016/j.jacl.2014.11.005. Epub 2014 Nov 28. PubMed PMID: 25911082.

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Thanks Michael!

 

(Psst: Dean, images as https, please!)

 

Sorry Michael. Are you referring to another thread? There weren't any images embedded in that post, only a YouTube video.

 

... it's the number of LDL particles (or rather (again), apoB-containing lipoproteins,) that ultimately drives disease, with LDL-C as a marker for LDL-P that works well for most people because the two are closely correlated, but that works poorly for people with extreme size distribution because it skews the normal relationship between LDL-C and particle number... 

 
Small, dense LDL particles are no more atherogenic than large ones: they are just surrogate markers for discordance between LDL-C and apoB/LDL-P, driven by insulin resistance and other underlying metabolic problems for all of which we have direct assessments.

 

So Krauss was mistaken and/or blowing smoke with his explanation that small LDL particles have their receptor site masked/occluded so they aren't cleared well by the liver as larger particles, and so they tend to hang around longer in the bloodstream, get oxidized and then get embedded in artery walls? Figures...

 

If it's just total number of LDL particles that matters for CVD risk, than it sounds like Krauss' new test, Cardio IQ® Lipoprotein Fractionation, Ion Mobility, which apparently measures both particle size and density by spraying a sample through the air to see how far the particles travel and on what trajectory, is a waste of money, even for those few individuals for whom LDL-C isn't a very good risk marker.

 

That is, if test apoB level and the result is misleadingly reassuringly low, the hidden risk will largely be caught if you have measures of insulin resistance and inflammation tested, and it's likely to occur in people whose LDL-C is low to begin with

 

Let me see if I've got this straight. So for someone like my medium-risk family member, whose LDL-C is borderline high and who is APOE4 positive, am I right in interpreting your bottom line as a recommendation to get an apoB test and combine that with LDL-C, fasting glucose (measure of insulin resistance) and CRP (measure of inflammation) to assess risk more accurately than LDL-C alone?

 

The important difference between consumption of dietary cholesterol, which has a negligible influence on heart disease risk, and cholesterol produced endogenously in the body (which can be a marker of risk, depending on a complete profile).

 

This is true for most people eating omnivorous diets, which contain significant amounts of SaFA and cholesterol, and elevated cholesterol because of overweight and lack of exercise, so the additional effect of an egg or two a day on circulating cholesterol is modest. However, if you have very low intake of these (eg, lacto-ovo vegetarians who don't get much cholesterol otherwise), the additional effect of dietary cholesterol (eg, from whole eggs) can be substantial, especially if you otherwise have a healthy lifestyle. 

 

In Todd's defense, he didn't make that statement up. He was quoting from the Rhonda / Krauss show notes.  But I really appreciate you clarifying the dietary cholesterol → serum cholesterol relationship Michael. 

 

Since the new USDA guidelines basically (and inappropriately IMO) let dietary cholesterol off the hook, I've been telling friends and family that the cholesterol in eggs doesn't appear to raise serum cholesterol because people's serum cholesterol is already too high, and is therefore less sensitive to being pushed higher by dietary cholesterol. But for people who eat an otherwise healthy diet and have a healthy lifestyle, dietary cholesterol can indeed push up serum cholesterol in an unhealthy way.

 

Surprisingly and for a change, you and Dr. Greger agree.  When you two are on the same page, I figure it must be true!

 

--Dean

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Todd,

looks like the cholesterol in eggs is not a problem because....

 

choline saves the day!!!

 

http://www.unisci.com/stories/20014/1029013.htm

 

Hallelujah! Choline to the rescue. The researchers even got a patent on the idea called Phosphatidylcholine compositions and methods for lowering intestinal absorption and plasma levels of cholesterol. I will note that their research was from 2001, long before it was known that the phosphatidycholine in eggs is probably harmful due to its link to TMAO. They let the patent lapse in 2008, and that's a good thing.

 

--Dean

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Dean, and all:
 

 

(Psst: Dean, images as https, please!)

 
Sorry Michael. Are you referring to another thread? There weren't any images embedded in that post, only a YouTube video.

 


That's because you moved the (goal)post ;) . I edited the https into the image per your prior carte blanche on the subject — one of several recent cases.
 

 

That is, if test apoB level and the result is misleadingly reassuringly low, the hidden risk will largely be caught if you have measures of insulin resistance and inflammation tested, and it's likely to occur in people whose LDL-C is low to begin with

 
Let me see if I've got this straight. So for someone like my medium-risk family member, whose LDL-C is borderline high and who is APOE4 positive, am I right in interpreting your bottom line as a recommendation to get an apoB test and combine that with LDL-C, fasting glucose (measure of insulin resistance) and CRP (measure of inflammation) to assess risk more accurately than LDL-C alone?

 

 
As a measure of insulin resistance, I would get fasting glucose and insulin, from which you can calculate QUICKI (apparently more accurately reflects whole-body insulin sensitivity than HOMA-IR), and then throw in TG, HDL, and HbA1c (tho' I was mildly dismayed but grateful to you for pointing out the unreliability of the latter) as secondary measures.
 

 

 

The important difference between consumption of dietary cholesterol, which has a negligible influence on heart disease risk, and cholesterol produced endogenously in the body (which can be a marker of risk, depending on a complete profile).

 
This is true for most people eating omnivorous diets, which contain significant amounts of SaFA and cholesterol, and elevated cholesterol because of overweight and lack of exercise, so the additional effect of an egg or two a day on circulating cholesterol is modest. However, if you have very low intake of these (eg, lacto-ovo vegetarians who don't get much cholesterol otherwise), the additional effect of dietary cholesterol (eg, from whole eggs) can be substantial, especially if you otherwise have a healthy lifestyle.

 

 
In Todd's defense, he didn't make that statement up. He was quoting from the Rhonda / Krauss show notes.

 

 
 Oh, I ccertainly didn't think he made that up: if he hadn't gotten it from Krauss, he could have gotten it from USDA. It's widely stated, in part because (as I said) it's actually true for the great majority of people ("sick population") , and in no small part because the egg industry has been hammering at it for > 3 decades now.
 

looks like the cholesterol in eggs is not a problem because....
 
choline saves the day!!!
 
http://www.unisci.com/stories/20014/1029013.htm

That's a mechanism explaining why you absorb less cholesterol from eggs than from pure cholesterol; it's no data on health outcomes.
 

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