After-eating effects: Carbohydrates vs. fats

25. November 2009 William Davis (17)
In the ongoing debate over whether it's fat or carbohydrate restriction that leads to weight loss and health, here's another study from the Oxford group examining the postprandial (after-eating) effects of a low-fat vs. low-carbohydrate diet. (Roberts R et al, 2008; full-text here.)

High-carbohydrate was defined as 15% protein; 10% fat; 75% carbohydrate (by calories), with starch:sugar 70:30.

High-fat was defined as 15% protein; 40% fat; 45% carbohydrate, with starch:sugar 70:30. (Yes, I know. By our standards, the "high-fat" diet was moderate-fat, moderate-carbohydrate--too high in carbohydrates.)

Blood was drawn over 6 hours following the test meal.




Roberts R et al. Am J Clin Nutr 2008

The upper left graph is the one of interest. Note that, after the high-carbohydrate diet (solid circles), triglyceride levels are twice that occurring after the high-fat diet (open circles). Triglycerides are a surrogate for chylomicron and VLDL postprandial lipoproteins; thus, after the high-carbohydrate diet, postprandial particles are present at much higher levels than after the high-fat diet. (It would have been interesting to have seen a true low-carbohydrate diet for comparison.) Also note that, not only are triglyceride levels higher after high-carbohydrate intake, but they remain sustained at the 6-hour mark, unlike the sharper decline after high-fat.

It's counterintuitive: Postprandial lipoproteins, you'd think, would be plentiful after ingesting a large quantity of fat, since fat must be absorbed via chylomicrons into the bloodstream. But it's carbohydrates (and obesity, a huge effect; more on that in future) that figure most prominently in determining the pattern and magnitude of postprandial triglycerides and lipoproteins. Much of this effect develops by way of de novo lipogenesis, the generation of new lipoproteins like VLDL after carbohydrate ingestion.

We also see this in our Track Your Plaque experience. Rather than formal postprandial meal-testing, we use intermediate-density lipoprotein (IDL) as our surrogate for postprandial measures. A low-carbohydrate diet reduces IDL dramatically, as do omega-3 fatty acids from fish oil.
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Comments (17) -

  • darnoconrad

    11/25/2009 3:19:52 PM |

    The Graphs are too small to read even when clicked on.

  • Robert McLeod

    11/25/2009 5:31:22 PM |

    It's not solely the fault of de novo lipogenesis, as even on a high fructose meal with radio-nucleotide labeled carbon in the fructose, only like 20 % of the triglycerides in the blood are from DNL.  Glucose consumption doesn't seem to result in DNL unless the liver is already full of glycogen.

    Insulin is known to down-regulate acylation stimulating peptide (ASP), which is the paracrine hormone that regulates uptake of lipoprotein (i.e. "cholesterol") micelles into fat cells.

  • Ms. X

    11/25/2009 5:46:34 PM |

    Dr. Mike Eades wrote a while back that fats, especially saturated fats go into the lymph system after digestion, and not immediately into the bloodstream.

    Why is it then that "since fat must be absorbed via chylomicrons into the bloodstream" is an "accepted" notion?  You implied it was wrong, without actually saying so...Do most medical practioners really not know how fat is absorbed into the body?

  • DrStrange

    11/25/2009 8:02:26 PM |

    You MUST look at this in context!  Excess dietary fat, especially saturated fat, causes insulin resistance.  It takes about 2 weeks of consistently eating approx 10% calories from fat, not more and not cheating, to remove that huge component of insulin resistance.  If the study were done in that context the results would be quite different.  How do I know?  I have done it several times on myself!!!

  • DrStrange

    11/25/2009 8:03:30 PM |

    oops, forget to request email follow-ups. So now I have.

  • TedHutchinson

    11/25/2009 10:42:41 PM |

    @ darnoconrad
    Dr Davis did say "full-text here hoping people would follow the link, download the PDF, and have their own copy to enlarge as required.

  • Stephan

    11/25/2009 10:42:41 PM |

    Hi Dr. Davis,

    Thanks for posting this.  It answered a question I've had for a while now.  The palmitate is interesting as well.

  • Helen

    11/26/2009 2:18:06 AM |

    Very interesting and kind of scary, with family members of mine with heart disease pounding down the carbs and cutting the fat.  

    I'm a bit confused by the Track Your Plaque Program, though.  In some of the info on the main site, saturated fats are described as inflammatory and something to be avoided.  But you seem to consider them okay - am I right?  And Dr. B G at AnimalPharm, who says she is counseling her clients with the TYP program, is big on saturated fats.  Can you explain the discrepancy?

  • Dr. William Davis

    11/26/2009 2:38:08 AM |

    Hi, Helen--

    The Track Your Plaque program stand on a number of issues, including saturated fat, has evolved over the years. We now do not restrict them, but nor do we suggest a carte blanche  approach, since we do continue to maintain rather strict LDL targets for plaque reversal.

    I believe that Dr. BG was expressing her own opinion in the Animal Pharm blog. While she's got plenty of great thoughts on this issue, it does not represent the "official" stand of the program.

  • Nigel Kinbrum BSc(Hons)Eng

    11/26/2009 9:18:52 AM |

    Is it possible that the higher fat diet hit an optimum fat/carb mixture, where carbs were low enough to keep fasting TGs low and fats weren't high enough to spike post-prandial TGs?

  • Dr. William Davis

    11/26/2009 2:51:39 PM |

    Hi, Nigel--

    Good question. Stay tuned--plenty more on this conversation to come.

    The entire world of postprandial metabolism is truly a fascinating, though complex area, that is only beginning to yield to investigation. The Oxford group has made enormous contributions to this understanding.

  • Anonymous

    11/27/2009 10:00:20 PM |

    Thanks for this, Gretchen, that's a lot of work!

    It's interesting that my husband's endocrinologist, whom he is seeing for high blood pressure, insists on non-fasting labs.  He has my husband get his tests (blood and urine) one hour after a meal.  He says the fasting tests are very misleading.

  • Helen

    11/28/2009 2:34:27 AM |

    Another question on saturated fats.  I know they raise LDL, and lately I've been reading that they raise the benign kind, not the vLDL.  But I have read in many places (including the Track Your Plaque article I mentioned) that they are "inflammatory."

    Is that a false accusation, confusing saturated fats with trans-fats (since hydrogenated fats were used in some experiments regarding saturated fats)?

    Or is it one of those things that depends - on other dietary factors or disease states, such as diabetes, etc.?  Or is it unknown?

    It's hard for me to believe that nature would only want us to eat monounsaturated and omega-3 fats (as omega-6's are inflammatory, too).  That would seem fairly limiting for an omnivore.  Of course, it could be a proportion thing, too.

  • StephenB

    11/30/2009 7:32:50 PM |

    Helen wrote:
    "Another question on saturated fats. I know they raise LDL"

    The above may not be true. There may be a small near term rise, but long term I don't believe they have no impact or even lower LDL. You might find this blog entry interesting.

  • Anonymous

    1/16/2010 1:25:20 PM |

    Rather interesting site you've got here. Thank you for it. I like such themes and anything that is connected to this matter. BTW, try to add some images Smile.

  • buy jeans

    11/3/2010 3:48:57 PM |

    It's counterintuitive: Postprandial lipoproteins, you'd think, would be plentiful after ingesting a large quantity of fat, since fat must be absorbed via chylomicrons into the bloodstream. But it's carbohydrates (and obesity, a huge effect; more on that in future) that figure most prominently in determining the pattern and magnitude of postprandial triglycerides and lipoproteins. Much of this effect develops by way of de novo lipogenesis, the generation of new lipoproteins like VLDL after carbohydrate ingestion.

  • simvastatin

    5/25/2011 5:22:39 PM |

    Consequently, one of the advantages of glucose and other carbohydrates is that they can enter into the oxidation process much more quickly and provide energy more rapidly.

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Non-profit hospitals

Non-profit hospitals

21. April 2007 William Davis (1)
Hospitals hide behind a veil of non-profit.

Ostensibly operating for the public good, most hospitals enjoy all the business advantages of non-profit status. This means that any profits that flow to the bottom line at the end of the year are not subject to tax. Hospitals point out that profit margins are modest, often ranging from 2-6%.

What they don’t tell you is that, regardless of non-profit status, lots of money can be paid out along the way. A hospital CEO who pays himself $4 million dollars a year can work for this non-profit organization. He can also direct the hospital in business expansion: pharmacies, extended-care facilities, medicine and medical supply distributorships. Your friendly hospital CEO, as well as his many administrators, can hold positions in hospital subsidiaries, complete with salaries and perks.

Yes, most hospitals are officially non-profit. But that’s a designation for tax purposes. It does not mean that hospitals are non-lucrative.

I believe that it’s time for hospitals to drop the façade of “Saint” in their names or other religious names—Methodist, Baptist, Jewish, All Saints’. More accurate would be something like “ABC Medical Enterprises, Inc.” That way, the public would be quicker to recognize that they are dealing with a business run by people eager to make more money.
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  • Gary Greenfield

    10/13/2007 9:03:00 AM |

    Wow, excellent insight and I wholeheartedly agree. I am of the opinion that post-modern man having abandoned an appreciation and concern  for the health of the soul has idolized the human body to such an excess that he is willing to pay any price to save his body while neglecting his own soul. The passions of those in the health care community are taking advantage of the passions of the misdirected patient. Both the physician and the patient have abandoned God and the anchor that historically kept medical care tied to a love for God and man failed long ago.  Now rather than being harbored in the peaceful waters of virtue and self sacrifice, we are shipwrecked on the rocks of greed and self love.

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Lies, damned lies, and statistics

Lies, damned lies, and statistics

18. April 2009 William Davis (8)
In the last Heart Scan Blog post, I discussed the question of whether statin drugs provide incremental benefit when excellent lipid values are already achieved without drugs.

But I admit that I was guilty of oversimplification.

One peculiar phenomenon is that, when plaque-causing small LDL particles are reduced or eliminated and leave relatively benign large LDL particles in their place, conventional calculated LDL overestimates true LDL.

In other words, eliminate wheat from your diet, lose 25 lbs. Small LDL is reduced as a result, leaving large LDL. Now the LDL cholesterol from your doctor's office overestimates the true value.

Anne raised this issue in her comment on the discussion:

I eliminated wheat - and all grains - from my diet nearly three years ago (I eat low carb Paleo). My fish oils give me a total of 1680 mg EPA and DHA per day, and my vitamin D levels since last year have varied between 50 ng/ml and 80 ng/ml. However, my lipid profile is not like either John's or Sam's:

LDL cholesterol 154 mg/dl
HDL cholesterol 93 mg/dl
Triglycerides 36 mg/dl
Total cholesterol 255 mg/dl

My cardiologist and endocrinologist are happy with my profile because they say the ratios are good, no one is asking me to take a statin. My calcium score is 0.


However, if we were to measure LDL, not just calculate it from the miserably inaccurate Friedewald equation, we would likely discover that her true LDL is far lower, certainly <100 mg/dl. (My preferred method is the bull's eye accurate NMR LDL particle number; alternatives include apoprotein B, the main apoprotein on LDL.)

So Anne, don't despair. You are yet another victim of the misleading inaccuracy of standard LDL cholesterol determination, a number that I believe should no longer be used at all, but eliminated. Unfortunately, it would further confuse your poor primary care doctor or cardiologist, who--still believe in the sanctity of LDL cholesterol.

By the way, the so-called "ratios" (i.e., total cholesterol to HDL and the like) are absurd notions of risk. Take weak statistical predictors, manipulate them, and try to squeeze better predictive value out of them. This is no better than suggesting that, since you've installed new brakes on your car, you no longer are at risk for a car accident. It may reduce risk, but there are too many other variables that have nothing to do with your new brakes. Likewise cholesterol ratios.
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Comments (8) -

  • Jeff

    4/18/2009 12:02:00 PM |

    I am in a similar boat.  I eliminated wheat, added cod liver oil(1-1.5 TBS or so per day), and take vitamin D supplements(gel caps around 4-5K IU per day).  Here were my results:

    TOTAL: 272
    HDL: 76
    LDL(calculated): 184
    Triglycerides: 62

    I strongly suspect the LDL is BS due to large particle size.  I will only be able to tell with the NMR, which I will do sometime this year.  I am not worried so I am in no rush.

  • arnoud

    4/18/2009 1:26:00 PM |

    Dr. Davis, thank you for providing such eye-opening insights in the interpretation of lipid testing results, and for explaining the limits of the usefulness of these measurements.

    However, in the typical doctor's office, the high (calculated) LDL prompts the doctor to push for treatment (including statins).  My doctor tells me that I need not avoid statins, as he is taking those himself, and he wouldn't if he'd think they were a problem.

    I can take my NMR Liposcience LDL particle count result to my doctor, and tell him that my real LDL number is 1/10th of the LDL particle count.  This actual number looks great!  How can I show my doctor that this calculation is correct (LDL particle count divided by 10), and that the standard Framingham calculated LDL should be ignored.   Is there a reference paper I can show my doctor, which explains the science behind the "LDL particle count divided by 10" rule?

  • john elfrank

    4/18/2009 1:35:00 PM |

    I had a coronary calcium scan a  few years ago. My score was about 350 with most of the calcium in the LAD.

    My Manhattan cardiologist responded by putting me on the treadmill and doing an eco stress test. I passed it with flying colors.


    I went to my internist who said  I should be concerned about that calcium score. I said my cardio won't give me any other tests. He said to go back and tell him I have chest pains. I did, got the angiogram and a stent for the 80% blockage in my "widow-maker" LAD.

    Now my lipid profile (I have dyslipidemia) is LDL 23, HDL 23, triglycerides 350 (1000 w/o meds). I had thyroidectomy in 1991 and take synthroid 200 mg.

    My combo thereapy is:
    2000 Niaspan, 40 Simvastatin, 200 Co-enzyme Q10, 1200 fish oil. It'a about as aggressive as my body can stand. Tricor and other fibrates interfere with synthroid absorption (I bet you didn't know that).

    My questions are:
    1. Would it be better for me to take the new combo Simvastatin/Niaspan drug rather than take them separately?

    2. Just passed a nuclear stress test. Should I insist on another angiogram soon?

    3. Would another calcium scan be useful?

    Thanks,

    John

  • sk

    4/18/2009 3:38:00 PM |

    this is absolutely spot on!  My numbers prior to NMR showed a total cholesterol of 150, HDL of 41, and TRG of 53.  Because of family history, my internist had me take NMR study and results showed that my particle number for LDL was 1795 and all small particles.  Since eliminating wheat and being on a statin my particle number is down to 1305,but still all small. Not sure that size can be changed, probably genetic.  
    Sadly, many out there think they have a fine profile from indirect measurement, and reality is that many probably do not.

  • Kiwi

    4/18/2009 10:05:00 PM |

    What is the recommended range for the ApoB test?
    My lab gives this:

    Male reference range 0.52 - 1.09 g/L
    Female reference range 0.49 - 1.03 g/L

    Using the Immunoturbidimetric method.
    VAP and NMR tests not available here.

    http://www.labnet.co.nz/testmanager/index.php?fuseaction=main.DisplayTest&testid=292

  • Dr. B G

    4/20/2009 9:42:00 PM |

    Anne,

    Those are FANTASTIC, phenomenal labs !!!

    You go GIRL!

    -G

  • Dr. B G

    4/20/2009 9:42:00 PM |

    Anne,

    Those are FANTASTIC, phenomenal labs !!!

    You go GIRL!

    -G

  • Ravi

    4/23/2009 9:42:00 AM |

    I strongly suspect the LDL is BS due to large particle size. I will only be able to tell with the NMR, which I will do sometime this year. I am not worried so I am in no rush.

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