Small LDL: Perfect index of carbohydrate intake

8. December 2009 William Davis (15)
Measuring the number of small LDL particles is the best index of carbohydrate intake I know of, better than even blood sugar and triglycerides.

In other words, increase carbohydrate intake and small LDL particles increase. Decrease carbohydrates and small LDL particles decrease.

Why?

Carbohydrates increase small LDL via a multistep process:

First step: Increased fatty acid and apoprotein B production in the liver, which leads to increased VLDL production. (Apoprotein B is the principal protein of VLDL and LDL)

Second step: Greater VLDL availability causes triglyceride-rich VLDL to interact with other particles, namely LDL and HDL, enriching them in triglycerides (via the action of cholesteryl-ester transfer protein, or CETP). Much VLDL is converted to LDL.

Third step: Triglyceride-rich LDL is "remodeled" by enzymes like hepatic lipase, which create small LDL.


Carbohydrates, especially if they contain fructose, also prolong the period of time that triglyceride-rich VLDL particles persist in the blood, allowing more time for VLDL to interact with LDL.

Many people are confused by this. "You mean to tell me that reducing carbohydrates reduces LDL cholesterol?" Yes, absolutely. While the world talks about cutting saturated fats and taking statin drugs, cutting carbohydrates, especially wheat (the most offensive of all), cornstarch, and sugars, is the real key to dropping LDL.

However, the effect will not be fully evident if you just look at the crude conventional calculated (Friedewald) LDL cholesterol. This is because restricting carbohydrates not only reduces small LDL, it also increases LDL particle size. This make the calculated Friedewald go up, or it blunts its decrease. Conventional calculated LDL will therefore either underestimate or even conceal the real LDL-reducing effect.

The reduction in LDL is readily apparent if you look at the superior measures, LDL particle number (by NMR) or apoprotein B. Dramatic reductions will be apparent with a reduction in carbohydrates.

Small LDL therefore serves as a sensitive index of carbohydrate intake, one that responds literally within hours of a change in food choices. Anyone following the crude Friedewald calculated LDL will likely not see this. This includes the thousands of clinical studies that rely on this unreliable measure and come to the conclusion that a low-fat diet reduces LDL cholesterol.
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Comments (15) -

  • nitrile exam gloves

    12/8/2009 3:58:05 AM |

    Thanks for the knowledge sharing...it helps to be healthy.

  • x.ds

    12/8/2009 12:02:31 PM |

    Here is a link showing the atherogenicity in mice of different saturated fats in diets with 1% cholesterol. Look at page 1416 of the free full report that can be downloaded here:

    http://www.ncbi.nlm.nih.gov/pubmed/8409772

    On the opposite you can see bread not being atherogenic in baboons here:

    http://www.ajcn.org/cgi/content/abstract/33/8/1869

    By the way you can notice the effect of 0.1% cholesterol at the end of the article = 1 gm cholesterol per kg of food = 5 egg yolks.

    Does it look a lot ? "There is evidence from animal experiments showing that if atherogenic dietary factors are reduced to levels comparable to man's intake, the same vessel changes occur as with higher levels, but more slowly."

    Download the free full report here:

    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1938976/

    In this report you can also see butter to be highly atherogenic to swine without additional cholesterol to their diet.

  • Bobber

    12/8/2009 5:06:03 PM |

    What about rice?  Does it also increase small LDL particles?

  • Nigel Kinbrum BSc(Hons)Eng

    12/8/2009 6:54:52 PM |

    @x.ds: Humans aren't C57BL/6J mice (susceptible to diet-induced fatty streak lesions), baboons or pigs.

  • Future Primitive

    12/8/2009 7:34:20 PM |

    @x.ds

    The strain of mice in the first study are predisposed to diet-induced obesity, type 2 diabetes, and atherosclerosis.

    Likewise, here's an interesting quote from the last paper based on a porcine model: "Whenever there are three
    animals from the same litter, they are divided equally among the three groups (ie, "control", "butter", & "egg yolk" groups)  In the present experiment, this occurred once. These three pigs had the most aortic atherosclerosis in their respective groups. The control pig with the most atherosclerosis was the brother of the pigs with the most disease fed egg and butter."  

    The group of pigs with the highest rate of atherosclerosis was the egg yolk group - yet at most we see a vanishingly positive relationship, if any, in a large number of human epidemiological studies of moderate egg consumption and heart disease (too many to list here - many are recent and easy to locate, though).  Do we even have grounds to formulate a hypothesis of egg induced atherogenesis based on human observational studies? I don't know, really - though a casual glance suggests, "no".

    Looking forward to reading the other study you pointed us to when I get the time.

  • Anonymous

    12/8/2009 7:42:17 PM |

    x.ds:

    Often times these animal studies don't translate well when applied to humans.

    Also, like Dr. Davis pointed out in his blog, most (LDL) cholesterol lowering research doesn't use advanced lipoprotein testing like NMR so the data is misleading to say the least.

  • Anonymous

    12/8/2009 9:16:54 PM |

    x.ds:

    It would be nice for a change to see experiments on other than herbivorous (mice) or mostly vegetarian animals (both pigs and baboons on the wild).

  • Dr. William Davis

    12/8/2009 11:48:34 PM |

    Bobber--

    While all carbohydrates increase small LDL, the effect of wheat is the most extravagant.

  • Anon X

    12/9/2009 3:18:19 AM |

    I generally agree with those who deny the universal applicability of experimental results in mice and rats to men. However, I do so with this one caveat; there is one fact I cannot deny: Many women are convinced that most men are rats.

  • LynP

    12/9/2009 4:42:51 AM |

    Doc, does this mean that I ca sorta log my particle size by getting my apoB checked in quarterly labs? I'll never be able to convince primary to do the outright particle size test...yet (working on that). Thnx.

  • Anonymous

    12/9/2009 3:08:55 PM |

    I admit I do not understand VLDL-C. What I would really like to find is a simple range scale. Mine shows up VLDL-C..7  Non HDL ..70
    I do not know if that is good or bad. Is there such a chart showing like,  1 good ... 100 bad ??
    LP(a) shows up by itself and I understand that because there is a range showing bad ..over 30.
    Any help understanding appreciated

  • David

    12/10/2009 2:39:45 AM |

    Dr. Davis,

    I honestly think you are doing God's work and have learned to appreciate the value of heart scans through your site.  However, it still bugs me that so many people in Asia can live off of large quantities of white rice with minimal atherosclerosis.  For instance, this study shows that American Whites have much higher atherosclerosis than Japanese despite the Japanese having much higher LDL-cholesterol, blood pressure, fasting glucose, and smoking rates:

    http://ije.oxfordjournals.org/cgi/content/full/34/1/173


    This other study (below) tries to explain this difference based on the Japanese consumption of fish. However, if you look at the data, those Americans who consume the most fish oil consume about as much fish oil as those Japanese that consume the least fish oil, and yet between these comparable groups in terms of fish consumption, the Japanese still have vastly lower atherosclerosis on heart scans.  And the Japanese American group consumes more fish than the White American group and has more coronary calcium.

    http://content.onlinejacc.org/cgi/content/full/52/6/417


    And here is another study showing much lower CAC in Japanese than in Japanese-Hawaiians even after controlling for a bunch of risk factors including fish intake:

    http://aje.oxfordjournals.org/cgi/content/full/166/11/1280


    Although in this other study looking at only at Americans, the incidence of CAC appears to be similar to that in Japanese - so maybe there was something unusual about the US samples in the other studies?

    http://content.onlinejacc.org/cgi/content/full/49/20/2013

  • Anonymous

    12/10/2009 8:23:46 PM |

    Dr. Davis,
    What is your opinion of the LP-Pla2 test for arterial plaque?  If you've used the test, do any elements of your program reduce levels of this enzyme?

  • buy jeans

    11/3/2010 9:44:57 PM |

    However, the effect will not be fully evident if you just look at the crude conventional calculated (Friedewald) LDL cholesterol. This is because restricting carbohydrates not only reduces small LDL, it also increases LDL particle size. This make the calculated Friedewald go up, or it blunts its decrease. Conventional calculated LDL will therefore either underestimate or even conceal the real LDL-reducing effect.

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