Saturated fat and large LDL

Here's a half-truth I often encounter in low-carb discussions:

Saturated fat increases large LDL particles

For those of you unfamiliar with the argument, I advocate a low-carbohydrate approach, specifically elimination of all wheat, cornstarch, and sugars, to reduce expression of the small LDL pattern (not to mention reduction of triglycerides, relief from acid reflux and irritable bowel, weight loss, various rashes, diabetes, etc). Small LDL particles have become the most common cause for heart disease in the U.S., exploding on the scene ever since agencies like the USDA and American Heart Association have been advising the public to increase consumption of "healthy whole grains."

This has led some to make the pronouncement that saturated fat increases large LDL, thereby representing a benign effect.

Is this true?

It is true, but only partly. Let me explain.

There are two general categories of factors causing small LDL particles: lifestyle (overweight, excess carbohydrates) and genetics (e.g., variants of the gene coding for cholesteryl-ester transfer protein, or CETP).

If small LDL is purely driven by excess carbohydrates, then adding saturated fat will reduce small LDL and increase large LDL.

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.

So to say that saturated fat increases large LDL is an oversimplification, one that can have dire consequences in the wrong situation.

Comments (44) -

  • Anonymous

    2/16/2010 10:02:36 PM |

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

  • Anonymous

    2/16/2010 11:02:49 PM |

    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?

  • Laura

    2/16/2010 11:37:17 PM |

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

  • Anonymous

    2/16/2010 11:43:41 PM |

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

  • Anonymous

    2/16/2010 11:46:43 PM |

    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

  • Daniel

    2/16/2010 11:50:11 PM |

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

  • jtkeith

    2/17/2010 12:26:14 AM |

    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!

  • David

    2/17/2010 12:38:19 AM |

    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?

  • Ellen

    2/17/2010 1:09:25 AM |

    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?

  • Harold

    2/17/2010 1:38:12 AM |

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

  • steve

    2/17/2010 1:49:56 AM |

    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!

  • Anonymous

    2/17/2010 1:50:56 AM |

    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?

  • switters

    2/17/2010 4:44:09 AM |

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

  • Paul

    2/17/2010 9:46:22 AM |

    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.

  • Rabbi HIrsch Meisels

    2/17/2010 2:14:23 PM |

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

  • zach

    2/17/2010 3:26:16 PM |

    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?

  • Alfredo E.

    2/17/2010 3:48:38 PM |

    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.

  • Anonymous

    2/17/2010 5:48:11 PM |

    Harold, I am also interested in the familial hypercholesterolemia question.  After a quick search, I found this 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.  


  • Anonymous

    2/17/2010 5:54:55 PM |

    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?  


  • Anonymous

    2/17/2010 7:04:29 PM |

    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.

  • Dr. William Davis

    2/17/2010 7:47:07 PM |

    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.

  • Scott Miller

    2/17/2010 8:46:27 PM |

    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.

  • Anonymous

    2/17/2010 9:08:19 PM |

    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.

  • Anonymous

    2/17/2010 10:27:45 PM |

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

  • Anonymous

    2/17/2010 11:09:09 PM |

    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.

  • Anonymous

    2/17/2010 11:10:11 PM |

    "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?

  • Kurt G. Harris MD

    2/18/2010 12:56:55 AM |

    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.

  • Dr. William Davis

    2/18/2010 1:52:52 AM |

    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.

  • Stephen

    2/18/2010 3:11:53 AM |

    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.

  • Anonymous

    2/18/2010 3:15:38 AM |

    How do you know how much small LDL you have?

  • Bonnie

    2/18/2010 3:53:00 AM |

    ""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.  


  • LeenaS

    2/18/2010 4:12:28 AM |

    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,

  • Mike

    2/18/2010 4:26:28 AM |

    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.

  • Kurt G. Harris MD

    2/18/2010 4:43:49 AM |

    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.

  • Paul

    2/18/2010 6:19:52 AM |

    Thin. Nice. I'm less concerned. lol

  • Anonymous

    2/18/2010 1:22:06 PM |

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

  • David

    2/19/2010 3:10:43 AM |

    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?


  • pmpctek

    3/7/2010 5:50:15 PM |

    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.

  • Anonymous

    4/19/2010 1:45:33 PM |

    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.

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    11/3/2010 6:44:37 PM |

    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.

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    11/3/2010 6:55:04 PM |

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

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