Is there an inexpensive way of finding out which form you have?

is there any truth to the idea that if your trig/HDL ratio is under 2.0 that your LDL type is predominantly large/buoyant?

Is there a way to determine whether small LDL production is carb- or genetics-caused?

Is this the same for poly/mono unsaturated fatty acids?

Dr. Davis,

Does the form of saturated fat have any impact on this in the case of genetic predisposition to small LDL formation? For example, does it matter if the fatty acids are lauric acid and stearic acid versus something like palmitic acid?

Rick Braden

Dr. Davis,
That's very interesting!!  Any chance you could provide the reference?
Thanks, Dan

This naturally leads to the question about understanding our personal genetic coding.  Without that coding information it seems difficult make an informed decision about the consequences of lowering carbohydrate and increasing fat (and saturated fat) until the consequences are upon you!

This definitely needs a follow-up post. I've not seen this distinction until now. If true, Dr. Davis, does it not present a difficult dilemma for those who have both genetic sdLDL and Lp(a)? If saturated fat needs to be restricted for genetically high sdLDL, would this not leave the Lp(a) (which responds best to saturated fat intake) unopposed? What is your proposal to address this?

Interesting post, Dr. Davis. How would one find out if they are genetically predisposed to react to saturated fat intake with an increase in small LDL?

Do you have some specific references for LDLa and saturated fat? Is it essentially congenital hypercholesterolemia that reacts with the sat fat?

this is a long overview discussion. thank you!  What would dietary recommendation be for someone if small LDL is genetic in origin?  Also, wouldn't this pattern possibly require statins to get LDL particle count as low as possible since it is unlikely that diet will do the job?  In my case, i need Lipitor and Zetia; otherwise my particle count mostly small remains high despite Vit D, normal weight,no wheat cornstarch or sugar.  Great post!

Doc -

Good post but -

Hard to understand post without the background basis on which the statement is made.

Is your statement based on clinical observations? Or is it based on opinion only?

Yes, references supporting your premise in this article would be very welcome.

This post concerns me because as a low carber I find it difficult to maintain a low carb diet without saturated fat sources. Perhaps this is driving the concern and questions from others also.

Count me in those who are waiting to see data where this is coming from.
Thanks for all your blogs posts.

Yes, I hope this isn't a hit and run post. Many learned people, such as Peter at hyperlipid would probably disagree. Do you have any references?

So what do we do if we should not eat but a few carbos and up to certain amount of protein?

The rest have to be saturated fats, isn't it?

Please, some more practical information before we all run over the cliff.

Harold, I am also interested in the familial hypercholesterolemia question.  After a quick search, I found this http://www.jlr.org/cgi/reprint/23/8/1196.pdf with a quote: "LDL has been
found to be cholesterol-enriched and triglyceride-poor
(5, 6), and in one study, the peak flotation rate of FH LDL
has been found to be higher than in normals (6),
implying decreased density, increased size, or both.
However, these results are difficult to assess, since there
is considerable heterogeneity of LDL in normal subjects,
although size, flotation rate, and composition"

So, FH people may be predisposed to large, fluffy LDL.  However, I do not know whether FHs handle saturated fats better than normals, and this is an important question.  

-Aaron

A question on triglycerides...if high TGs are a trigger for small, dense LDL and should be minimized, are there any ways to reduce area-under-the-curve TGs after a meal (other than the usual low carb, omega-3, etc. recommendations).  Are large, infrequent meals better than small, frequent meals?  Does fiber change the shape of the post-meal TG curve?

Also, does fasting TG tell the whole story?  Could one have, say, <50 mg/dL fasting TG but have elevated TG throughout the day as a result of large, high-fat meals?  

-Aaron

Thank you Dr. Davis!  Finally a voice of sanity in this whole sat fat hoopla.

I for one, although not neurotic about it, do not favor saturated fats and will eat a good non-hydrogenated margarine (like Smart Balance) over butter any day.

Please keep up this sane blog and give us the WHOLE enchilada, not just what some want to hear.

Search PubMed or Google Scholar and you will find NO data on this issue. To my knowledge, there are none that distinguish genetically -driven small LDL vs. lifestyle-induced.

This is based on having tested lipoproteins in thousands of people over the past 10+ years.

Prototypical "genetic small LDL" person: 5 ft 10 inch, 140 lb male who eats low-carb. In other words this person is at ideal weight and does not eat foods that trigger small LDL--yet has 90% small LDL by NMR (e.g., 1200 nmol/L, LDL particle number 1550 nmol/L). Should this person overindulge in saturated fat, small LDL will go up.

Dr. Davis, how do you know it is saturated fats that are the cause? For example, most low-carbers also have elevated intake of inflammatory polyunsaturated fatty acids, which I would be much more likely to blame.  But, in either case, it seems there are too many uncontrolled variables involved (as far as food intake) to pin any of them to the wall.

It's very difficult for me to believe saturated fat is the cause, while other possibilities exist.

For everyone worrying about this, just get yourself a VAP or NMR test.  If you have LP(a) or sdLDL, that will show it.  You don't need genetic testing.

What's are the trig and HDL numbers for the prototypical "genetic small LDL" person?

Thanks Dr. Davis for another insightful post from your clinical experience, giving the kind of information that helps elucidate why saturated fat works for some and not for others - and the kind of information you can't get anywhere else.  Ignore the pro saturated fat/anti-polyunsaturated fat zealots, who can't be persuaded by any evidence or logic.

"What's are the trig and HDL numbers for the prototypical "genetic small LDL" person?"

I'd like to second that - can one have high HDL and low trigs and still have a small LDL pattern?

Hello Dr. Davis

You said:

"Should this person overindulge in saturated fat, small LDL will go up."

Just to be clear, are you saying you have observed low carb subjects (how low?) that have added saturated fat to their diets and then on subsequent testing you have seen sdLDL rise in absolute and percentage terms?

If they were truly LC, were they already high sat fat at the time of the NMR or were they high PUFA (South Beach?)

May I ask how many such cases you have seen?

You should definitely publish this, or if you don't think it is publishable maybe you could give us all the data in a blog post.

Thanks, this is very interesting.

In people with presumptive genetically-determined small LDL, HDL can be 70 mg/dl or greater, triglycerides 45 mg/dl or less, yet small LDL persists, usually at 600 nmol/L (NMR).

I have approximately 100 patients like this. They tend to be very thin with BMI's of 23 or so, yet small LDL persists.

Hi Dr. Davis,

This post really intrigues me. I am a first year medical student (24 yo) with familial hypercholesterolemia. I am on a low carb paleo diet, taking omega 3, vit D and just recently added magnesium to the mix as well. I went off Lipitor two months ago just an experiment to go along with this new eating plan, and received blood work only a few days ago. Numbers about 450 on total and 285 for LDL. My CT scan already showed plaque buildup in the coronary arteries, aorta, and one valve. While I am not looking for medical advice per se (since I know you prefer not to give it over your blog) I was just curious as to how your track the plaque plan and recommendations are effected with this type of genetic disorder. My cardiologist says if I dont go on drugs immediately I'll have a cardiac event at 40 years of age. I could use some advice and direction to persue. Is it impossible to avoid genetics, and the use of drugs are unavoidable? Thanks. Really appreciate it.

How do you know how much small LDL you have?

""I'd like to second that - can one have high HDL and low trigs and still have a small LDL pattern?""

Well - just speaking for myself, I have high HDL and low trigs, and always had a mix of small/large (A/B) pattern LDL.  When I stopped eating wheat, my LDL all became large.  

I also have high Lp(a), which was uneffected by my eliminating wheat.

You can drive yourself crazy figuring out what's OK to eat and what's not.  I don't worry about it anymore.  I rarely eat wheat because I've seen results from Not eating it, try not to overdo the sugar and fruit, get plenty of veggies and protein.  

I get my VAP test once or twice a year to make sure everything is where it should be, more or less.

I'm just not going to worry about it beyond that.  

Bonnie

Dr. Harris:

Are these customers of yours lean lowcarbers eating plenty of LA or very, very much protein in their diet? If not, then what do they eat?

With regards,
LeenaS

Interesting, and concerning, since I fit that description:

Chol: 6.35mmol/L
HDL: 1.88
LDL: 4.2
Triglycerides: 0.66
Chol/HDL ratio: 3.4
American Values:  TG 58.47 LDL 162.54 HDL 72.75
Triglyceride/HDL ratio: 0.8
Hieght: 6'0
Wieght: 165lbs
BF 8%

I've had other opinions on these numbers; should I be pursuing more accurate particle numbers?  I go out of my way to consume large amounts of red meat, coconut oil, butter, and eggs.  I'm fitter and healthier (subjectively) than I ever have been at 36 than I was in my 20's.  I find it disconcerting than I could potentially be doing something detrimental.

Hi Dr. Davis

In the original post you said:

"saturated fat will increase small LDL.  In other words, saturated fat tends to increase the dominant or genetically-determined form of LDL."

So, if I follow this correctly, you are saying that these 100 patients all had increases in their sdLDL after documented increases in saturated fat in their diets? In other words you had two data points for each subject, correct?

If the subjects did not all have documented increases in sLDL then by "persist", do you mean their sdLDL went down with LC eating (like 800 to 600, say) or do you just mean that they had a single high value and it was only measured once, but it was high?

If it is the latter, I could see how it's fair to say that some LC eaters have a higher sdLDL than we might predict (for whatever reason) but it seems like a non sequiter to conclude that the sdLDL would be made higher with more sat fat consumption.

I just want to make sure I get this straight so I understand it correctly.

Thin. Nice. I'm less concerned. lol

Does this group of people also have elevated blood sugar, as might be predicted by another of your blog postings?

http://heartscanblog.blogspot.com/2009/12/to-track-small-ldl-track-blood-sugar.html

Dr. Davis,

I concur with Dr. Harris in that more details would be nice to better understand exactly what you're saying.

Are other variables accounted for? Were many, most, or all of these patients on statin drugs, which could have prevented a shift in particle size if triglycerides were low and insulin sensitivity was high?

Again, if there is such a phenomenon going on, is the "genetic sdLDL" clearly atherogenic in the same way that "environmental sdLDL" seems to be?

If so, I ask again, what is the solution for someone who is afflicted by both Lp(a) and genetic sdLDL? The "profile" for genetic sdLDL is similar to the profile for those with Lp(a), and there is probably a lot of crossover. Saturated fat lowers Lp(a), but (presumably) raises genetic sdLDL. This is a fierce dilemma! Would not the better choice be to choose the diet that opposes the more vicious of the two, which is Lp(a)? What is the priority?

Has a high SFA diet only increased sdLDL per NMR, or has it also clearly been shown to increase CAC scores? In other words, does it clearly progress the disease itself?

David

Saturated fats not linked to heart disease: Meta-analysis - American Society for Clinical Nutrition (January 13, 2010). doi:10.3945/ajcn.2009.27725 © 2010

It would really be interesting to know what the primary sources of saturated fat are for these "100 patients".  There may be a single (widely available) common source of sat fat that these specific patients are consuming, do we even know that?  I agree, by what has been revealed, that there are too many variables to know conclusively that saturated fat is the cause of their persistently elevated small LDL.

Mark me down as someone who is not convinced that CLA, n3 rich organic, free range, and wild animal sources of fat could possibly in any way be detrimental to anyone.

When will people stop worrying about cholesterol numbers? They really don't mean anything.

Until someone explains a plausible mechanism through which lipoproteins directly kill me I will ignore it any suggestion that they do. This is what a good scientist would do.

@ Rick Braden
Re does it matter if the fatty acids are lauric acid and stearic acid versus something like palmitic acid?
Palmitate is the predominant saturated fatty acid in soybean oil. Soybean oil increases total cholesterol,LDL and LDL:HDL ratio, whilst HDL diminished.
Coconut oil (predominantly Lauric acid) does not cause dyslipidemia and promotes a reduction in abdominal obesity.

That is generally the case,  stearate does not appear to increase LDL... Laurate and stearate reduce the total cholesterol/HDL ratio

I don't know if the genetic predisposition to LDL alters response to laurate, stearate palmitate.

It may help people better understand the difference in cholesterol forms if they look at the photos of VLDL, LDL, HDL,  NED KOCK has kindly provided on his blog

If, on the other hand, your small LDL is genetically programmed, then saturated fat will increase small LDL. In other words, saturated fat tends to increase the dominant or genetically-determined form of LDL. If your dominant genetically-determined form is small, then saturated fat increases small LDL particles.

buy jeans: I'd love to see clinical evidence supporting that claim.

Heart diseases are a major matter of concern these days therefore all that can be done to correct the diet and make it benefit good health should be taken to.

Dietary Carbohydrate Modifies the Inverse Association Between Saturated Fat Intake and Cholesterol on Very Low-Density Lipoproteins
Interesting full text free paper that may change the way saturated fat is viewed. I wonder if the source of the Saturated fat (butter/coconut oil as opposed to indoor grain fed beef/lard) and the type of carbohydrate (Wheat sweet potato)  may add a further level of complication.

re: " Her dose: 6000 mg of a standard 1000 mg capsule (6 capsules) to provide 1800 mg EPA + DHA, the effective omega-3 fatty acids."

Excellent blog entry! On fish oil, this dose seems to be very high. Do you recommend this as a typical regimen?

On another related topic, your views on common statins (eg lipitor, crestor, zocor, etc) would be appreciated. I'm getting strong warnings from knowledgable friends that statins are dangerous for liver function and can cause irreversiable damage. On the other hand I personally have found them to be very effective in bringing my cholesteral numbers in line, more than anything else I've tried. TIA

John--
No. This dose is for treatment of high triglycerides or postprandial disorders. Our usual starting dose is 4000 mg (1200 mg EPA+DHA).

Regarding the statin issue. I'd refer you to an article I wrote for Life Extension magazine  archived on their website, www.lef.com. The article, entitled Cholesterol and Statin Drugs: Separating Hype from Reality, can be accessed at http://search.lef.org/cgi-src-bin/MsmGo.exe?grab_id=0&page_id=1044&query=davis%20statin&hiword=DAVI%20DAVID%20DAVIE%20DAVIES%20DAVIN%20DAVIO%20DAVISON%20DAVISS%20DAVIT%20STATI%20STATING%20STATINS%20STATIS%20davis%20statin%20

I just read your article that you referred to in your previous comment answer.

I was on statins several years ago. Not only did I experience muscle and joint pains, I also had serious memory problems, depression and sleep problems. I also found that my long-standing "restless legs syndrome" became much much worse. I've also talked to many people who have experienced serious PND (peripheral nerve disorders).

What I also experinced was a rather significant drop in HDL cholesterol.

Thoughts?

"But Phyllis is not terribly good at following advice. She likes to wander off and follow her own path. She noticed that the healthy bread sold at the grocery store and containing flaxseed boasted "900 mg of omega-3s per slice!". So she ate two slices of the flaxseed-containing bread per day and dropped the fish oil."

Allow me to defend Phyllis. If all she had been told was to take a given amount of omega-3s, then she was following the prescribed path. She should have been educated as to what the various omega-3s are and which type she needed to consume.

Thank you for passing on your article 'Statin Drugs: Separating Hype from Reality'... very informative I must say! Just a quick heads up on your comment about folic acid (ie “always take folic acid and vitamin B12 with niacin to protect against disruption of healthy methylation patterns”), although studies are not conclusive, apparently folate therapy (taking a combination of folic acid, vitamin B6, and vitamin B12) may be harmful after stent placement and probably should be avoided. For those who have this condition it’s advised instead, to try to get enough vitamin B by eating a balanced diet. [ref: Lange H, et al. (2004). Folate therapy and in-stent restenosis after coronary stenting. New England Journal of Medicine, 350(26): 2673–2681]

I have to chime in here regarding Cindy's comment on statins:

I dutifully tried for nearly two years to tolerate the various statins prescribed by my doctor.  The deep muscle aches and spasms were nearly unbearable... getting far worse when my "numbers" still weren't right and he decided to DOUBLE my dosage of Vytorin (Zocor + Zetia) from 10/20 to 10/40.  What resulted was a true nightmare for me.  I terminated this med when I had such severe muscle aching, spasms and dis-coordination that navigating up a flight of stairs was nearly impossible.  Not only that, but my memory was (fortunately temporarily) impaired, and I can remember little from a three month period of time.  Interestingly my CK was never elevated and this all happened while taking 200mgs. daily of a very reputable Co -Q10 formulation.  Cessation of the Vytorin saw the aches subside within 2 or 3 days and full mental clarity resumed within a week.  I was lucky.

My doctor stated that there were three other statins we hadn't yet tried... fat chance doc!

What chaps me is that the pharmaceutical companies continue to state that there is only a small percentage of patients who have side effects.  In practice, LOTS of people have problems tolerating statins, BUT these things never are reported, certainly mine wasn't by my doctor.

Side effects can be reported to the UCSD Statin Study, and to the FDA.  The FDA form is unduly cumbersone and frankly, unless you nearly died, it probably isn't worth the time.  The UCSD Statin Study questionnaire is very thorough... and as soon as I get some time I'm planning to report my experiences with statins to them.

I am not optimistic that doing either of the above will change the statistical misinformation out there on statin side effects.  The pharmaceutical giants have too many billions at stake to ever allow this information to attain credibility.  Their advertising billions shout otherwise...

Great meds, IF they work for you without problems.  For me they appear to be deadly, so I think I'll just stick with the other strategies, including niacin, fish oil, etc., etc. that I've learned through TYP.

madcook

I have to chime in here regarding Cindy's comment on statins:

I dutifully tried for nearly two years to tolerate the various statins prescribed by my doctor.  The deep muscle aches and spasms were nearly unbearable... getting far worse when my "numbers" still weren't right and he decided to DOUBLE my dosage of Vytorin (Zocor + Zetia) from 10/20 to 10/40.  What resulted was a true nightmare for me.  I terminated this med when I had such severe muscle aching, spasms and dis-coordination that navigating up a flight of stairs was nearly impossible.  Not only that, but my memory was (fortunately temporarily) impaired, and I can remember little from a three month period of time.  Interestingly my CK was never elevated and this all happened while taking 200mgs. daily of a very reputable Co -Q10 formulation.  Cessation of the Vytorin saw the aches subside within 2 or 3 days and full mental clarity resumed within a week.  I was lucky.

My doctor stated that there were three other statins we hadn't yet tried... fat chance doc!

What chaps me is that the pharmaceutical companies continue to state that there is only a small percentage of patients who have side effects.  In practice, LOTS of people have problems tolerating statins, BUT these things never are reported, certainly mine wasn't by my doctor.

Side effects can be reported to the UCSD Statin Study, and to the FDA.  The FDA form is unduly cumbersone and frankly, unless you nearly died, it probably isn't worth the time.  The UCSD Statin Study questionnaire is very thorough... and as soon as I get some time I'm planning to report my experiences with statins to them.

I am not optimistic that doing either of the above will change the statistical misinformation out there on statin side effects.  The pharmaceutical giants have too many billions at stake to ever allow this information to attain credibility.  Their advertising billions shout otherwise...

Great meds, IF they work for you without problems.  For me they appear to be deadly, so I think I'll just stick with the other strategies, including niacin, fish oil, etc., etc. that I've learned through TYP.

madcook

RE: Madcook's comment "Side effects can be reported to the UCSD Statin Study, and to the FDA. "

I'm wondering if the 'UCSD Statin Study' provide summary reports on submission findings?

BTW, his note is a very interesting personal account which echos mine to a certain extent, albeit I'm seemingly in the early stages. I'm starting to have pretty severe shoulder pain coming out of nowhere after six mths on Zocor. I've started taking Q-10 (re: your rec) to see if it helps. Previously my reaction to Lipidor was almost immediate with severe skin rash symptoms.