Eat triglycerides

Dietary fats, from olive oil to cocoa butter to beef tallow, are made of triglycerides.

Triglycerides are simply three ("tri-") fatty acids attached to a glycerol backbone. Glycerol is a simple 3-carbon molecule that readily binds fatty acids. Fatty acids, of course, can be saturated, polyunsaturated, and monounsaturated.

Once ingested, the action of the pancreatic enzyme, pancreatic lipase, along with bile acids secreted by the gallbladder, remove triglycerides from glycerol. Triglycerides pass through the intestinal wall and are "repackaged" into large complex triglyceride-rich (about 90% triglycerides) molecules called chylomicrons, which then pass into the lymphatic system, then to the bloodstream. The liver takes up chylomicrons, removes triglycerides which are then repackaged into triglyceride-rich very low-density lipoproteins (VLDL).

So eating triglycerides increases blood levels of triglycerides, repackaged as chylomicrons and VLDL.

Many physicians are frightened of dietary triglycerides, i.e, fats, for fear it will increase blood levels of triglycerides. It's true: Consuming triglycerides does indeed increase blood levels of triglycerides--but only a little bit. Following a fat-rich meal of, say, a 3-egg omelet with 2 tablespoons of olive oil and 2 oz whole milk mozzarella cheese (total 55 grams triglycerides), blood triglycerides will increase modestly. A typical response would be an increase from 60 mg/dl to 80 mg/dl--an increase, but quite small.

Counterintuitively, it's the foods that convert to triglycerides in the liver that send triglycerides up, not 20 mg/dl, but 200, 400, or 1000 mg/dl or more. What foods convert to triglycerides in the liver? Carbohydrates.

After swallowing a piece of multigrain bread, for instance, carbohydrates are released by salivary and gastric amylase, yielding glucose molecules. Glucose is rapidly absorbed through the intestinal tract and into the liver. The liver is magnificently efficient at storing carbohydrate calories by converting them to the body's principal currency of energy, triglycerides, via the process of de novo lipogenesis, the alchemy of converting glucose into triglycerides for storage. The effect is not immediate; it may require many hours for the liver to do its thing, increasing blood triglycerides many hours after the carbohydrate meal.

This explains why people who follow low-fat diets typically have high triglyceride levels--despite limited ingestion of triglycerides. When I cut my calories from fat to 10% or less--a very strict low-fat diet--my triglycerides are 350 mg/dl. When I slash my carbohydrates to 40-50 grams per day but ingest unlimited triglycerides like olive oil, raw nuts, whole milk cheese, fish oil and fish, etc., my triglycerides are 50 mg/dl.

Don't be afraid of triglycerides. But be very careful with the foods that convert to triglycerides: carbohydrates.








Comments (31) -

  • Kurt

    6/8/2011 2:51:47 AM |

    There must be genetic variations, though, as my triglycerides have measured between 78 and 90 on every test since 1993. For the past two years, I've been eating a 20% fat diet (with about 50% carbs), and on my latest VAP test, my triglycerides were 78. The diet, by the way, lowered my LDL 30%.

  • Ian Goldsmid

    6/8/2011 2:55:47 AM |

    Dr. Davis

    Could you please clarify:

    If I have one slice of gluten free mixed grain /seed toast - and very liberally heap Organic Coconut Oil & Almond Butter on it - am I still going to get the exaggerated carbohydrate to triglyceride conversion effect from the toast?

    Thanks, IJG

  • Gene K

    6/8/2011 3:28:45 AM |

    Dr Davis,

    How much TG-rich foods is it safe for APOE 4 people to consume? Will this amount depend on their fasting TG? Will it be per meal or a day's total?

    Thank you.

  • Markus Damian

    6/8/2011 7:16:16 AM |

    I think this article is excatly on target- I ate a low-fat, high-carb vegetarian diet for years, and at one point my measured triglyceride levels were > 300. After I started omitting most refined carbs from my diet (and upping my fat/protein intake correspondingly), my last reading has been 88. So, for me at least, dietary intake of triglycerides is not substantially related to blood levels.

  • Markus D

    6/8/2011 7:32:02 AM |

    ... having said that, there is something which I don't quite understand. Given that virtually the entire human population is on a high-carb feast, it must be that some of us react differently to high-carb diet than others, otherwise everyone would have elevated triglyc levels, right? My mother, who is certainly genetically quite close to me, eats a high-carb, low-fat diet, and her triglyceride levels are normal ...  Many thanks, M.

  • Might-o'chondri-AL

    6/9/2011 12:18:07 AM |

    EPA (eicosa-pentaenoic fatty acid)  an omega-3  poly-unsaturated fatty acid reduces the amount of glucose that is made into tri-glycerides ("trigs") , thus decreasing de-novo lipo-genesis put out by the liver.  When I added daily concentrated fish oil  with 1,500 mg EPA & 750 mg DHA to my moderate carb diet my NMR  tested measurement of trigs went from 90 mg/dL down to 42 mg trigs/dL (tests  were 4 months apart).  

    EPA also increases the amount of insulin related glucose transporters inside skeletal muscle cells, which allays insulin resistance;  it (EPA) induces the skeletal muscles to "burn" more glucose for ATP energy  in oxidative phosphorylation , which decreases irritating lactate output that contributes to body "aches".  Insulin in circulation can then also work as a co-fact0r with EPA,  together they go on to increase functional  leptin  levels  (leptin = anti-appetite);  thus  we get less impulse to "graze"   between meals on  carbs that make  trigs.

  • carb sane

    6/9/2011 11:57:11 AM |

    Actually, it has been established that DNL is NOT a major source of fatty acids in VLDL.

  • majkinetor

    6/9/2011 1:49:40 PM |

    Actually, its around 20%

  • majkinetor

    6/9/2011 1:49:59 PM |

    Nice. I didn't know that. Thats pretty big amount of EPA/DHA, it is therapeutic amount often used for COX-2 inhibition.

    Can you tell more about the dosage ? Did you try smaller dose ? Is it fish oil or fish capsule or simply fish ? What are you thoughts about potential problems with PUFA and oxidation in regard to fish oil ?

  • carb sane

    6/9/2011 5:05:24 PM |

    Firstly, that's not about VLDL.  Secondly, that means around 80% comes from dietary fat.    Did you read my link?

  • Might-0'chondri-AL

    6/9/2011 6:15:27 PM |

    Hi majkinetor,
    I only went from no fish oil supplementation as an experiment to taking 1 tsp of Natural Factor's "pharmaceutical grade"  (  concentrated Canadian product's total fish oil=4,400 mg.  with 2,630 Omega 3 fatty acids of which 1,500 = EPA & 750 = DHA)  taken, as free  poured liquid along with morning food and evening food in 1/2 tsp measuring spoon slurps. Intake  of liquid oil was at the same time ate carbs , and carb intake was similar for when had 1st measured trigs when wasn't supplementing with fish oil  .  

    I personally don't think PUFA oxidation is an issue in diets that have lots of substrate for gut bacteria to make short chain 4 carbon fatty acid butyrate. It (butyrate) up-regulates many distinct  GST (glutathione S-transferase) genes;  these go on to tackle multiple lipid peroxidation by-products  (ex:  activity neutralizes 4-hydroxy- nonenal &  trans-alk-enals/dienals ),  while  micro-somal GST promotes the glutathione conjugation to electro-philes  which then can act to decrease lipid hydro-peroxide activity.

  • majkinetor

    6/10/2011 7:25:50 AM |

    Ah, sorry, I missread your post.

  • majkinetor

    6/10/2011 7:30:08 AM |

    Secondly, that means around 80% comes from dietary fat
    Not at all.
    80% from dietary fat AND cho.

  • Jimmy

    6/10/2011 11:11:24 AM |

    Might: Do you live in Canada?

  • Helen

    6/10/2011 11:25:24 AM |


    I used to take fish oil, but now that I'm measuring my glucose daily, I find that even a small dose immediately raises my fasting glucose 10-15mg, and somewhat worsens my post-prandial readings.  My own observation is in keeping a study that showed that prediabetic women's glucose control was worsened by a fish oil supplement.  (I don't have the link handy.)  Can you explain?

    I have the same troubles with modest supplements of vitamin C and niacin, though I'm sure for different reasons.  I find it interesting, and I don't mean that in any coded way, that two of Dr. Davis' recommended supplements  (fish oil and niacin) impair glucose control in me and in some studies.  I am wondering if this might explain in part his advice to shun carbs.  In the context of those supplements, carbs are not well tolerated.

  • Dr. William Davis

    6/10/2011 12:12:00 PM |

    Several commenters make the point that there is genetic variation in susceptibility to triglyceride intake and carbohydrate intake.

    Absolutely. Two people on the same diet can have wildly different results. Part of this is attributable to apo E genotype, apo C genotype, lipoprotein lipase and hepatic lipase genotypes, among others. Body weight and previous eating habits will also enter the equation. However, in most people increased triglyceride intake does not result in substantial increase in serum triglycerides.

  • Might-o'chondri-AL

    6/10/2011 9:59:19 PM |

    Hi Helen,
    I've heard some respond as you mention;  I wonder if they were all overweight during the data collection period, as pre-diabetic could imply.  In your circumstances (ie: blood glucose goes up with supplements)  it would be instructive to know if  you've a tendency for excess weight.

    My own niacin use went from none to 3x per day of 500 mg.  niacin taken with meals;   my own 2011 NMR lipid tests done 4 months apart were as follows.  Without any niacin fasting NMR cholesterol test results:  LDL = 139,  HDL=45,  total number of LDL particles  = 1,676,  with the number of small LDL particles  = 1,021 nmol/dL .  As for NMR cholesterol test with 1,500 mg daily total  niacin :  LDL = 100, HDL = 64,  total number of LDL particles = 976 , with the number of small LDL particles = nmol/dL.

    The nice plunge in small LDL doesn't seem to be due to a massive restriction of carbs;  in fact,  both my  HbA1c  and fasting serum glucose test result ciphers  went up slightly after I had  instituted niacin &  EPA/DHA fish oil  (started both at same time).   Incidentally,  I've never had  weight gain problems  and unintentionally lost 10 pounds I didn't intend to  since started taking the fish oil;  losing so much small LDL was more than thought possible and maybe wasn't 100% due to the niacin  (also daily  added  6,000 IU vitamin D3 from none, taken as 2,000 IU  with each meal).

    So,  before you decide that niacin & EPA/DHA supplements driving up your post-prandial glucose is positively detrimental it might be good to have your own baseline data (ie:  NMR for cholesterol & HbA1c for accretion of  blood sugar) .  If you are in the USA you can get a valid blood draw order in ANY state at all and the emailed results by using  cheapest online arrangement from ;  their doctor orders the blood test for you and,  of course, I have no financial interest in this .

  • Might-o'chondri-AL

    6/10/2011 10:04:42 PM |

    see 2nd paragraph's last sentence to Helen above, missing number in last set of data is for number of small LDL nmol/dL and should be 96 (ninety-six) ... in other words  that data shows that with niacin the  small LDL  "plunged" to 96 from being 1,021 nmol/dL without niacin supplementation.

  • Helen

    6/11/2011 5:27:07 AM |

    Hi M-Al,

    I'm different from a lot of visitors to this blog in that I have never had cholesterol problems.  I don't remember my exact numbers but my HDL and LDL split has been deemed "ideal," and my triglycerides range from 44-48, with total cholesterol being about 157.  

    My current BMI is 20 or less (haven't checked the charts lately) and my highest ever was 25, about a year ago.  Generally, I've been in the 23 range.  So, no, I don't have a propensity to weight gain.  On the other hand, I'm borderline diabetic.  Last year, at my highest BMI, my A1C was 6.4.  On low-carb, it slowly got down to 6.0, and my last test, on low-fat, was also 6.0, although according to my meter readings, taken at least three times a day, it should be 5.3.  I'm definitely right on the border with the diabetes, though have pushed it back some over the past year.  My blood sugar *sometimes* shoots to 200 or over within the first hour of eating (a "diabetic" number, though my endocrinologist says it has to be 200 at two hours to be considered clinical diabetes), but it quickly goes down again.  My liver seems to pump out a lot of glucose.  I tend to have a fasting glucose between 109 and 125.  Sometimes it gets as low as 99.  On low-carb, it ranged from 125 to 145, and was 160 a few times.  

    Needless to say, my biggest concern is my glucose level.  Metformin didn't help, low-carb didn't help much (and definitely made my tolerance for any amount of carbs next to zero - I once went to 198 on a carrot and half an orange, but I don't anymore.  It also gave me heart palpitations, worsened my insomnia, and greatly impaired my exercise tolerance), and I wonder if I'm just stuck with what I've got at this point.  Not that I'm throwing in the towel.  Fortunately, my cholesterol profile has  been ideal, my resting heart rate and blood pressure are low-normal, and my weight is okay without a struggle.  But I'm getting aches and pains in my joints and think the fish oil could help there.

  • Peter

    6/11/2011 1:32:44 PM |

    Dr. Davis, at one point you were concerned that you were eating too many nuts
    because your ratio of omega 3 and 6 was off.  What is your current thinking about the trade-offs?

  • Might-o'chondri-AL

    6/11/2011 10:02:26 PM |

    Hi Helen,
    lost 2 replies, says server error ... sorry

  • Might-o'chondri-AL

    6/11/2011 10:14:46 PM |

    Hmm Helen,
    Sounds like epigenetic or good old genetic polymorphism ... appears that Hexokinase II (HK II) is NOT staying inside skeletal muscle mitochondria and glucose-6-phosphate (G-6-P) is working to keep HK II in cell cytosol in a loop,  whereby HK II engenders glycogen output and instigates lots of G-6-P ... that cell has own glucose from glycogen so GLUT 4 (glucose transporters) move too far away to pick up blood glucose  ... liver glycogen  for it's part involves HK IV (glucokinase) and G-6-P too, but may not be root of  your syndrome ... too slow a rate of G-6-P degradation and /or too many carbon or nitrogen terminals on HK II would allow G-6-P to yank HK II  into metabolism cranking out glycogen ...  hey - twice wrote this already.

  • Might-o'chondri-AL

    6/12/2011 12:49:42 AM |

    Helen, Hi-
    Metaformin probably did not work for you because it functions to increase glucose uptake by provoking anaerobic glycolysis to create additional glucose demand;   you may already be doing plenty  of anaerobic glycolysis  as a consequence of your extra ordinary local glycogen synthesis.  The carbon from glucose with anaerobic glycolysis engenders a lot of lactate being produced; your aching joints and body pain syndrome fit the profile of excessive lactate in circulation.

    There is no easy way to determine what phase of the G-6-P dynamic with Hexokinase forms is not working normally, if even involved.  When we wean to real food our skeletal muscles start to run glucose metabolism with HK II and GLUT 4,  rather than the HK I and GLUT 1  we started with;  this change over occurs when we  starts to relatively "burn" both carbs and fats  and skeletal muscles develop  their insulin sensitivity.

    I am not  a clinician, and you have your personal physician to guide you; if I had a distorted  HK II  and G-6-P pattern ( that was unresponsive to low carbs)  I would try to end run it,  and not have skeletal muscle cells utilizing glucose to stop ratcheting up G-6-P and short out the negative feedback loop . I'd  significantly increase my consumption of  dietary fat in the explicit form of unheated virgin coconut oil  and fatty fish (for the EPA/DHA);  if taking EPA causes  blood sugar to rise it is probably because the EPA is driving skeletal muscles to "burn" fat , and thus skeletal muscles are using less of the HK II glycogen  which itself then used even less blood glucose as substrate  (ie: EPA  reduces blood glucose commonly used so glucose level in blood measures higher if cell metabolism aberrant  in the manner like I surmise).

  • Might-o'chondri-AL

    6/12/2011 4:28:39 AM |

    Hi Jim,
    Am not  residing in Canada.

  • majkinetor

    6/12/2011 7:04:12 AM |

    Vitamin C can give falsely higher values when measuring bunch of markers, most notably glucose. Its because it is so similar with glucose (very similar net formula, the same transporters in the body - GLUT, its made from glucose in animals etc...)

    About oil, it can only slow down carb absorption and let the body tolerate better. Did you experiment with other fish oil manufacturers ? Perhaps something in the product apart from fish oil makes you feel that way. For instance, ascorbyl palmitate is typical antioxidant used (along with Vitamin E) so this can be responsible for false higher reading.

  • majkinetor

    6/12/2011 7:22:27 AM |

    Helen, did you try megadosing with Vitamin C (~10g per day as frequent as you can). Vitamin C influences beta cells in the pancreas and deficiency is common in diabetes. Scorbutic guinea pigs show defects in insulin metabolism in vitro. Higher glucose levels compete with C for transporter. Add chromium if you didn't. Daily exercise will surely help. Since low carb made your glucose problem worst (most probable is higher hepatic insulin resistance that is consequence of low carb diet) you might try to return some safe starches back (for instance potato or rice) and keep CHO between 50 and 75 g per day.  Ashes and pains in the joint might be consequence of your too low carb diet since carbs are used for joint functions. Carbs are also used for intestinal mucus which so on very low carb you might have some micronutrient deficiencies.

  • Dee

    6/13/2011 7:47:05 PM |

    Have you tried adding D-ribose to your mix of supplements?  It has helped with my muscle aches from exercise.

  • Kris - Health Blog

    6/14/2011 7:52:50 AM |

    It seems that a lot of doctors would do well by going back a few years in time and re-reading Biochem 101.

  • Jim Anderson

    6/14/2011 7:05:22 PM |

    My wife and I have both been following a low-carb eating plan.  For me, that has meant increased fat consumption from the start.  I have felt full and satisfied after meals, and can go longer without feeling hungry.  I have also lost weight steadily.  My wife, however, has had a harder time of it.   She claims that is because women just have a harder time losing weight than men do.  That's true, I guess, in general, but I have also noticed that she seems to be avoiding fat a lot more than I do.  (Well, I don't avoid it at all!)  So she gets hungrier more often.  It is very difficult to overcome years and years of anti-dietary fat propaganda!

  • Joe Lindley

    6/30/2011 2:04:03 PM |

    Yes!  Thanks for the complete explanation of the fats vs. carbs impact.  I'm successfully on a low carb diet now after quitting Atkins years ago because my wife was worried I'd keep over from a heart attack.  With the right information out there now that dietary fat won't hurt you, people can stick to a low carb diet and get enough satiety (food satisfaction) with fats in the diet to stay on a diet.  It's truly been a disaster that the nutrition authorities shooed us away from dietary fats starting in the 1970s.  It's taken decades to get the word out that dietary fats are OK.  I published a nostalgic post on this about how Barney Fife got it right back in 1963:

  • James Roberts

    7/30/2011 12:59:43 AM |

    Great post, great site.  I made my way to focusing on triglycerides by starting with Lipitor.  I had some bad though serious side effects (mostly insomnia),  so I dropped it and worked really hard on reducing fat intake.  That pretty much worked, but surprise (to me)... triglycerides went way up.  Now that I've also worked on cutting empty calories my levels are down to borderline.  Once you make it to a genuinely healthy diet everything seems to work out Wink