What's that in your mouth?

7. January 2010 William Davis (17)



Fat = triglycerides

In other words, eat fat, whether it's saturated, hydrogenated, polyunsaturated, or monounsaturated, and blood levels of triglycerides will go up over the next 6 hours. This remains true if there are carbohydrates in the meal, or if there are NO carbohydrates in the meal. It also remains true if you chronically consume fats.

While fats are the primary determinant of postprandial (after-eating) triglycerides, carbohydrates are the primary determinant of fasting triglycerides.

So, if your triglycerides are high on a fasting cholesterol (lipid) panel, it's most likely because you overconsume carbohydrates.


Thanks to cartoonist Eli Stein, who has generously allowed me to reprint his artwork on these pages. Mr. Stein has published his work in dozens of magazines and newspapers, including the Wall Street Journal, Barron's, and Good Housekeeping. More of his work can be found at Eli Stein Cartoons.
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Comments (17) -

  • Aaron Blaisdell

    1/7/2010 7:58:19 PM |

    Amen, brother! This is the dirty little secret that proponents of the lipid-hypothesis of CAD continually try to sweep under the rug. Looks like the cat's out of the bag, though, thanks to the internet.

  • Anonymous

    1/7/2010 8:23:51 PM |

    But what can be done about post-meal elevated triglycerides?  Would it be best to avoid fats too, and just eat fruits and vegetables, if one had the will power to do it?

  • Kiwi

    1/8/2010 8:24:56 AM |

    Perhaps we should just give up eating altogether.

  • Nigel Kinbrum BSc(Hons)Eng

    1/8/2010 10:41:14 AM |

    I think that worrying about post-meal elevated triglycerides is probably shortening your life more than post-meal elevated triglycerides.

  • Lindsay

    1/8/2010 2:44:33 PM |

    so what does this mean?

  • Emily

    1/8/2010 4:31:21 PM |

    "It also remains true if you chronically consume fats."

    my understanding is that it is actually in support of normal metabolic functioning for us to "chronically" eat fat. low carb eating, in my lay-person's opinion, means therefore eating good fats (and i am of the un-pc standpoint that saturated animalfats are a-ok) , not just green veggies alone. low-car and low-fat would be no fun! but that's just my 2 cents.

  • ET

    1/8/2010 7:12:24 PM |

    I've had two non-fasting cholesterol tests performed in the last year.  My fasting triglycerides are around 40.  My triglycerides three hours after eating a meal with 10g carbs and 59g of fat were 91.  The time prior to that, they were 79 eight hours after breakfast and three hours after lunch (both were high-fat meals).

    Yeah, they go up, but not that much.

  • donny

    1/8/2010 7:37:28 PM |

    So what about the other side of the equation? Decreasing the absorption rate of fat (or spreading it out over more meals) might not help any. But if you can optimize the deposition of fat where it really belongs, in subcutaneous fat tissue-- that is, if fat is deposited in fat tissue where it belongs until needed, at a rate close to the rate at which new dietary fat is absorbed into the bloodstream-- then there shouldn't be a problem.
    Interventions that raise HDL generally increase adiponectin. Eating less wheat, beer, fructose, or adding in fish oil, niacin, vitamin d, even being born a woman. And they also associate with less wheat belly.

    http://www.springerlink.com/content/dpy09vbc0r8jxnm9/

    -----------------------------------
    Conclusion/interpretation. These data suggest that adiponectin concentrations are determined by intra-abdominal fat mass, with additional independent effects of age and sex. Adiponectin could link intra-abdominal fat with insulin resistance and an atherogenic lipoprotein profile.
    --------------------------------
    Maybe they've got cause and effect reversed here? I read a study in mice that were leptin-deficient. Adding extra adiponectin made the mice fatter. So adiponectin is probably not so much a reaction to deposited fat as it is a promoter, maybe a facilitator of proper fat storage.

    ?

  • Anonymous

    1/8/2010 7:44:30 PM |

    Thanks, interesting post. Just wondering: what about proteins?

  • Finn

    1/8/2010 8:58:31 PM |

    So if I eat cheese slices with butter as snacks all day, my triglys will be chronically high and I can get heart problems?

    Does this mean that intermittent fasting is very important if you eat low carb/paleo style?

  • Johnny M

    1/8/2010 10:41:07 PM |

    Where Oh Where can I find a Doctor like Doctor Davis in the New Jersey area?

    My doc who is a cardiologist referred to by local medicenter when it was found out my Trigs were 235 and Total Cholesterol were 295, LDL 195, HDL 57, promptly put me on 5 mg Crestor to lower trigs and LDL, never discussed diet or anything with me. His office plastered with Pfizer Lipitor posters and Crestor bags given by pharma reps.

    Heres the kicker, this was all done with blood work that was NON-FASTING. I had blood drawn an hour after I had eaten eggs and bacon. This was also around halloween time too when I was over indulging on ALOT of Sub sandwiches and bread and lots and lots of candy. I love peanut butter cups. But I know 5 a day is excessive, which was my intake.  Was I getting a DOUBLE Whammy increasing my Trigs?

    Since I found this blog, I've been taking my Crestor which I don't want too. But have taken up the no wheat diet and HFC out of my diet that Dr Davis suggests. Dropped 18 pounds in a matter of weeks.

    Took my own cholesterol with one of those home machines after 4 weeks of Crestor. Doctor wants to test after 3 months. But my Total Cholesterol was 151, calculated LDL 87, HDL 50 and Trigs 69. I wonder how much was the Crestor doing the change or the change in my diet and 18 pound weight loss?

    Sorry for the rambling, but Dr. Davis your blog does give great info and brings peace of mind to me.

  • Bryce

    1/8/2010 11:34:10 PM |

    Anonymous,

    Absolutely not. Having elevated triglycerides immediately after a meal is not a dangerous thing. It's only when they are chronically elevated that you are in danger. Same thing with insulin. Chronically elevated levels are the problem.

    Both of these are caused by excessive sugar/carb consumption.

    -Bryce Lee

  • Anonymous

    1/9/2010 2:37:00 AM |

    Bookmarked this. Sometimes non-standard due to you after sharing. Positively value my time.

  • Dennis

    1/9/2010 4:34:05 PM |

    Dr. Davis: a friend of mine recently had triglycerides trending up to 700 and more. I pointed him to your blog, recommended low carbs and fish oil, and after *one month* his TGs are around 200.

    Kudos to you.

  • Scott W

    1/9/2010 5:51:41 PM |

    Interesting series of posts. But keep one thing in mind: Excess blood glucose is converted to palmitic acid by the liver...a saturated fat.

    (This fact alone should give the anti-saturated-fat crowd pause...if the body could have evolved to convert glucose to any type of fat, why did it evolve to produce a saturated fat? Can't be too bad for you...)

    Anyway, if the body through DNL produces a saturated/healthy fat after only a very brief (and normal) spike in blood glucose - after which the glucose returns to a normal fasting level - then high starch (not fructose) diet appears to be quite healthy. This would answer the question of why a rice-base culture can maintain good health while consuming a diet high in starches...in effect, they are eating a high saturated fat diet.

    If they don't eat continuously, allowing their bodies time to eliminate the excess blood glucose and the attendant insulin spike before the DNL triglycerides (palmitic acid) hits their blood stream, then there is no insulin-driven storage of the fats. Instead, they have elevated blood-borne fats that remain available for a consistent energy source of over time, of a type that their body prefers and has evolved to produce.

    Can you get the same effect from eating saturated fat in the first place? Yes. But to assume that this is better than the starch-driven approach you have to accept that higher levels of ANY saturated fat in the bloodstream is unhealthy. Which runs counter to the viewpoint of paleo and low-carb eaters.

    As Stephen has pointed out, there is no evidence that post-prandial glucose spikes are dangerous to someone with a healthy metabolism (i.e. not a type I or II diabetic). So, if there is no evidence of danger from a post-starch-meal spike, why would your body care where it got its saturated fat? Either dietary or liver-produced, it’s all the same once it is in your blood.

    Following the chain of reasoning further, a high-starch diet that leads to DNL production of palmitic acid would be healthier than a high fat diet composed of vegetable oil or other undesirable fats.

    We have to be very careful about quickly latching onto bits of "evidence" that confirm our biases. Remain scientific, think it through. The human body is an amazingly complex organism; when we begin to isolate its responses to prove our points, we can start down a path that leads to conclusions that may satisfy our dietary worldview, but are not entirely accurate.

    Scott W

    Note: If we are being carefully scientific in our approach, we should be careful to distinguish our descriptive terms for non-fat and non-protein calorie sources. "Carbohydrates" is too general. It encompasses fructose, which as a much different effect on the liver than glucose. My discussion above focuses on starches for a reason; they break down to glucose, which the body has evolved to handle efficiently, even in large quantities. It can handle fructose, too, but did not experience it in large quantities prior to modern times. Even using the term "sugar" is inaccurate, since it is half fructose and half glucose. By extension of my discussion above, eating pure glucose powder (dextrose) would be as healthy for a rice-based culture as eating white rice itself. You are simply giving the body the end product of rice digestion (glucose), from which it can produce palmitic acid.

  • Dr. William Davis

    1/9/2010 9:19:15 PM |

    There's no question that postprandial triglyceride-rich lipoproteins are causally related to atherosclerosis, regardless of whether they were fat-driven or carbohydrate-driven.

    However, these brief posts are NOT meant to endorse low-fat diets. They are meant to show that a simple low-fat vs. low-carb approach is too simple-minded. There are other aspects of diet that count for substantial effects. Postprandial phenomena are one important class of effects that cannot be fully controlled by just controlling carbohydrate or fat content of the diet.

  • Anonymous

    1/9/2010 9:47:39 PM |

    You still haven't explained why the chart in your previous post (Di Novo Lipo-what?), where normoinsulinemic people have lower DNL on a high-fat diet, is in marked contrast to the chart of Gretchen in the post before that (Gretchen's postprandial diet experiment II) when she was eating high-fat.  From those two posts, it seems that peoples' postprandial triglyceride level is dependent on the amount of insulin they produce (and obviously how sensitive they are to that insulin).  Therefore a high-fat diet is not problematic unless one is also hyperinsulinemic.

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