Butter and insulin

In a previous post, Atkins Diet: Common Errors, I commented on butter's unusual ability to provoke insulin responses. I offer this as a possible reason why, after a period of effective weight loss on a low-carbohydrate program, inclusion of some foods, such as butter, will trigger weight gain or stall weight loss efforts.

This develops because of butter's insulin-triggering effect, doubling or tripling insulin responses (postprandial area-under-the-curve). If insulin is triggered, fat gain follows.

Here's one such study documenting this effect: Distinctive postprandial modulation of ß cell function and insulin sensitivity by dietary fats: monounsaturated compared with saturated fatty acids

López et al 2008

From Lopez et al 2008. Mean (± SD) plasma glucose, insulin, triglyceride, and free fatty acid (FFA) concentrations during glucose and triglyceride tolerance test meal (GTTTM) with no fat (control), enriched in monounsaturated fatty acids (MUFAs) from refined olive oil (ROO meal), with added butter, with a mixture of vegetable and fish oils (VEFO) or with high-palmitic sunflower oil (HPSO). N = 14.

The postprandial (after-eating) area-under-the-curve is substantially greater when butter is included in the mixed composition meal. This effect is not unique to butter, but is shared by most other dairy products.

Fat, in general, does not make you fat. But butter makes you fat.

Comments (83) -

  • Miki

    3/19/2010 5:48:56 PM |

    I wander if the effect is due to the milk solids or the type of fatty acids. If it is the milk solids making ghee will solve the problem.

  • Anonymous

    3/19/2010 5:54:39 PM |

    So the low fat control meal of pasta and bread gives the LEAST amount of insulin response!

    So, to avoid insulin spikes you must minimize all types of fats.

    Fat+Pasta seem to trigger the insulin.  The glucose response does not seem to matter all that much.

  • jd

    3/19/2010 5:54:39 PM |

    Thanks for the great info as always.

    Is it correct to say, in view of the graphs, that this type of dairy-induced insulin elevation is not mirrored by blood glucose readings, so we couldn't check for it at home with a glucose meter?

  • John

    3/19/2010 5:56:08 PM |

    butyric acid causes an insulin response, as does casein...interestingly, although i can't find it, i saw a paper that showed the insulin response to white bread was actually less when combined with butter...

  • daniel the smith

    3/19/2010 6:06:21 PM |

    What if you eat it without any carbs (e.g., like I do with my eggs in the morning)? If there's nothing to trigger the insulin in the first place, butter can't make it worse, right? Or am I wrong?

  • Lucy

    3/19/2010 6:16:20 PM |

    That's an interesting study indeed.  It seems to indicate that eating no fat at all (the control meal) provided better results in every category except glucose rise, and then it was only with the rest of a fairly tight pack.  Adding any fat at all spiked the insulin significantly higher.   This is consistent with the charts in your post "The Timing of Blood Sugars".  Yet you concluded there that carbohydrates should never be consumed without fat.  Based on these studies, it sure looks like a person is trading a little glucose rise for a larger insulin spike when consuming fat.  Which begs the question, which is worse?  Does insulin cause more problems than glucose?   You did say it was the insulin that triggered weight gain...

    I remain unconvinced that I should rush out and follow Ornish.

  • Diana Hsieh

    3/19/2010 6:34:54 PM |

    Interesting post -- and my experience confirms it.  Here's something that I recently posted to the OEvolve e-mail list:

    As folks might know, I've been struggling with my weight due to my hypothyroidism.  Even though many of my symptoms have improved, I continued to gain weight at the very consistent rate of 3 pounds per month.  Sometimes, mostly due to a bit of fasting, I'd be down a pound or two, but then I'd suddenly gain back all that weight plus more within a day or two, so that I'd be on that steady upward slope again.  

    In late February, I was up to just over 150 pounds; that was my pre-paleo weight.  That's not so terrible in and of itself -- although I hated it -- but the continued upward progression was really alarming.  Plus, I'd outgrown almost all my pants!

    After listening to Robb Wolf talk about the growth-promoting, insulin-spiking effects of dairy, I realized that I'd been eating a huge amount of dairy lately -- far more than ever before.  I've been buying those huge blocks of cheese from Costco, not to mention those delectable half gallons of cream.  So instead of eating meat-and-veggie leftovers for lunch, I was usually eating some high-fat dairy.  And for breakfast, I would eat cheese rather than meat with my eggs.  

    A few weeks ago, I decided to cut my dairy down dramatically -- to basically just one serving per day at most.  So I'll have a cup of raw milk kefir or cheese on meatza, but not much more than that.  That was really hard for me to do for the first week, as I really was used to eating it as a staple.  I'm also not eating nuts, absent some "must have food as I run out the door" emergency, as I know they can hamper weight loss for me.

    The results have been good so far.  I've not gained any more weight in the last two weeks.  Instead, I've lost four pounds.  Given what I had been experiencing, that's pretty remarkable.

    I'm not sure how much more weight I'll lose just due to cutting back the dairy.  I definitely think my metabolism isn't quite up to speed yet due to the hypothyroidism. However, my experience suggests that eating boatloads of dairy -- even good-quality, high-fat dairy -- is an excellent way to gain weight.

    That being said, I don't think that it's necessary to cut out all dairy to lose weight.  I'm still eating some dairy, and I'm losing weight.  Plus, I lost my original 18 pounds with my 1.5 shares of raw milk -- that's 1.5 gallons per week.  (I'm now down to just 1/2 shares, meaning 1/2 gallon per week.)  I just think dairy is something to consider reducing if you're not meeting your weight loss goals.


    I've not lost much more weight since writing that, but I'm definitely not gaining any weight.  That's huge: I was petrified that I'd be 200 pounds by next summer.  

    I've probably stalled in that weight loss because my metabolism is still screwy due to my not-yet-fully-managed hypothyroidism.  Plus, I'm not seriously trying to lose weight right now: I don't want to stress my already over-stressed body.  But perhaps cutting out dairy entirely would make a difference.

    Anyway, thanks for putting some science behind my experience, Dr. Davis!  I'll definitely add a link to it in the discussion of dairy on the principles page of Modern Paleo.

    -- Diana Hsieh (Modern Paleo)

  • StephenB

    3/19/2010 6:40:08 PM |

    My working assumption has been that I don't need to worry about any increased insulin resistance with high saturated fat intake since I don't eat foods which spike my glucose. Am I correct?

  • Darrin Carlson

    3/19/2010 6:47:03 PM |

    Yikes! Never would have thought butter could do this. Are there any other non-carbohydrate foods that are known to cause insulin secretion?

  • Christian W

    3/19/2010 6:47:03 PM |

    If anything, it seems like the study supports the idea that all fats are bad, doesn't it?

    The zero fat control meal does better than all the fatty meals. Look at insulin for instance.

  • howardh

    3/19/2010 7:54:46 PM |

    I notice that you conveniently ignored the pasta (sugar/gluten) in the study, and attributed ALL of the negative effects to butter. Try again, this one failed.

  • Anonymous

    3/19/2010 8:35:11 PM |

    Hmmmm, Wheat Pasta and Wheat Bread?
    All bets are off. Would be curious to have conducted tests without either of those included.

  • Andrew

    3/19/2010 8:46:58 PM |

    Could butter still make you fat if you're eating below BMR?  It seems to me that if you were eating 1000 calories per day consisting of only butter, and your BMR was 1800, you would still lose weight.  Is there anything that scientifically proves this to be false?

  • Nostril Damus

    3/19/2010 9:00:35 PM |

    Any ideas why ?

    I believe insulin drives the rate of ageing, and this would certainly make me scale back my butter consumption.  

    But what part of butter causes this ?

  • Marielize

    3/19/2010 9:02:16 PM |

    Dear Dr Williams, I find this topic very interesting, but being a lay person would like to know a bit more. What would the "meal" they talk about be? Would that be grains? Is the resuls they got from combining grains with cream or butter? Would butter or dairy products have the same effect in the absence of grains?

  • Donald Duck

    3/19/2010 9:35:38 PM |

    Doesn't this study mainly show that butter is a bad idea when eaten together with lots of carbs?

    Is it really likely you would get the same insulin response if the butter was eaten without all that carbs?

  • Mark

    3/19/2010 9:44:04 PM |

    After removing dairy, grains, and anything else processed. I'd imagine it would be hard to eat too many calories when all you're left is meat, veggies, and fruit but not too much. Just curious, is that all we have to choose from?

  • K Walt

    3/19/2010 10:26:25 PM |


    But the meals were carb-heavy, too.

    "The subjects then ingested, within 15 min, a fat-rich meal consisting of dietary fat [50 g/m2 body surface area of butter, refined olive oil (ROO), high-palmitic sunflower oil (HPSO) or a mixture of vegetable and fish oils (VEFO) along with a portion of plain pasta (30 g/m2 body surface area), one slice of brown bread, and one container of skim yogurt.

    I wonder if the same effect would be noted if were JUST butter, or oil.

    Is it the butter? Or the wheat pasta, brown wheat bread and lactosey yogurt?

  • sonagi92

    3/19/2010 10:26:26 PM |

    Thanks for taking the time to post a response to inquiring commenters.

  • pyker

    3/19/2010 10:26:26 PM |

    Interesting. Here are the numbers from the study for insulin AUC:

    19960 +- 2766 control
    27970 +- 2107 VEFO
    29619 +- 4975 MUFA
    34749 +- 1167 HPSO
    37582 +- 4364 SFA (butter!)

    Unless I've misread the study, the "control" meal has no fat at all, and is not isocaloric with the test meals. "the macronutrient profile was as follows: 72% fat, 22% carbohydrate, and 6% protein (see Table S1 under "Supplemental data" in the online issue). The subjects also consumed the same test meal containing no fat as a control meal". So the butter test meal has nearly 4x as many calories as the control meal. The AUC for insulin between the two is about double for the butter, but that seems like a useless measure.

    Comparing like-for-like, the spread between average insulin AUC for butter meal and the isocaloric alternate fat meals  shows the butter to be about 34% higher than VEFO and only 8% higher than HPSO. (I have to be pedantic here and point out the spread between averages is not as good as would be the average spread, but I can't get that unless I have the raw data from the study.)

    If you want to claim that butter has some unique ability to raise insulin vs. other fats, this is not strong support.

    You say "butter's insulin-triggering effect, doubling or tripling insulin responses", and "butter makes you fat". I don't see support for either claim when I read that study.

  • Neonomide

    3/19/2010 10:44:24 PM |

    Why ?

    How about cream and fatty milk, or other dairy products ?

    I guess coconut is again the safest bet here...

  • Beth@WeightMaven

    3/19/2010 10:58:06 PM |

    I'm not an MD nor a research scientist. But decades ago, I was a math major. If I read the study and do my math right, the subjects ate an 800 kcal meal of which 72% was fat, for 576 kcals worth of fat (the other control meal components were pasta, bread, and skim milk yogurt).

    576 kcals worth is nearly 6T of butter -- or 3/4 of a stick! To me, that is important additional context for the increased AUC for both the insulin and the triglycerides.

    Considering my typical use (~1T/meal) and considering the potential downside of replacing carb calories with more PUFAs (and omega 6s -- even 1T of EVOO has over 1g of omega 6), I'm not ready to throw out my ghee just yet.

  • Cheryl

    3/19/2010 11:43:30 PM |

    Is it the milk solids that do it?  if so, then ghee may be an alternative.

  • Anonymous

    3/20/2010 12:52:10 AM |

    as a  personal anecdote - eating butter (even in amounts of 200 g. a day) speeds up my fat loss - i feel as if i'm burning inside (elevated metabolism?)...

  • Dr. William Davis

    3/20/2010 12:56:53 AM |

    I see that I touched a nerve.

    This study is not meant to stand on its own, but taken in the context of other studies.

    I think that you should eat butter . . . in small quantities and occasionally. I do not believe that the data argue for liberal use every day, or else you chance triggering insulin. Remember: It's the interpretation of the data in the context of the broader experience that leads you to practical conclusions.

  • Catherine

    3/20/2010 1:39:53 AM |

    What about coconut oil as a butter substitute? There is a lot of hype and hoopla about it being a "safe" medium-chain saturated fat to use as a butter substitute.  Anyone tested if it spikes glucose?

  • zach

    3/20/2010 3:57:00 AM |

    Pastured butter rocks. My belief with butter is "a stick a day keeps the doctor away."

    It's as though the more butter I eat the leaner I get!

    The anthropological evidence really contradicts the data you and loren cordain cite. The pancreases of many people in traditional cultures carried them toward 100 years old, reacting to dairy every day, multiple times per day.

    Here is a 112 year old woman from a very long lived people who use dairy as a staple.


  • Sue

    3/20/2010 7:49:50 AM |

    "Fat, in general, does not make you fat. But butter makes you fat."

    Why make such a comment in regards to butter?

  • Adam

    3/20/2010 8:18:10 AM |

    Dr Davis.

    First of all, thank you for your wonderful site and your willingness to impart life changing and saving advice for anyone to access.

    Peter at hyperlipid has written a counter on this particular blog entry of your.

    Would you care to comment?


  • CK

    3/20/2010 8:42:10 AM |

    So let me get this straight: Ingesting carbohydrates including the bad guy wheat does not do much to blood glucose levels and insulin response. But adding fat to the mix at least doubles, or, in the case of butter, quadruples the peak insulin response? That seems like the best refutation of all the low carb/paleo/primal/ef approaches I've ever seen. So where is the catch?

  • Anonymous

    3/20/2010 9:15:05 AM |

    The last sentence made me cry.

  • Donald Duck

    3/20/2010 9:54:54 AM |

    It seems like butter (or cream) without carbs does not create insulin spikes according to the study that Peter at Hyperlipid discusses here:


  • Anonymous

    3/20/2010 10:39:02 AM |

    If you eat fat, ASP levels will rise, which will make you gain fat. ASP levels increase in response to an oral fat load, and ASP is one of the most potent stimulant of triglyceride synthesis.

    So, if you eat carbs, insulin secretes and you store it as fat, if you eat fat, ASP levels rise and you store it as fat. Why is it only the insulin's fault?


  • But I thought...

    3/20/2010 11:03:43 AM |

    The oracle's take on your post doc:


  • Lori Miller

    3/20/2010 2:08:13 PM |

    I don't know about the effect of butter, but when I eat a fatty meal (like a cheesy omelet with an avacado), my BG goes down several points.

  • kilton9

    3/20/2010 2:23:42 PM |

    Here's a study that isolates cream and shows a very small insulin response: http://drbganimalpharm.blogspot.com/2009/12/insulin-and-aging-how-paleo-works.html

  • Alfredo E.

    3/20/2010 3:01:02 PM |

    This is becoming more confusing by the minute. First, no carbs,only fats and protein.

    Now, no butter, no dairy, no, carbs, just a few drops of fat and protein.

    I am going to cry, like the previous poster.

  • Hilary

    3/20/2010 3:05:41 PM |

    "Fat, in general, does not make you fat. But butter makes you fat."

    This seems wrong. When I eat more butter, I lose fat/weight. Eat more carbs, gain fat/weight. Been noticing this for years. Sure, put a load of butter on noodles or rice, and you'll gain plenty, but just keep the carbs low and there's no problem. This seems like a case of being blinded by science. Maybe the science isn't exactly wrong, but just incomplete or misapplied.

  • pmpctek

    3/20/2010 3:05:41 PM |

    I think I fugured it out...

    The AMA or AHA has kidnapped Dr Davis and they are forcing him to post these confusing refutations.

    What will we see next?  Studies that show how Cocoa Puffs actually will help reach our 60-60-60 goal after all?

  • Joseph

    3/20/2010 3:07:15 PM |

    After reading your post and the hyperlipid post I'm left with a few questions.

    1.The big one, why is butter raising insulin so much? I had previously thought it was only high GI carbs that did that. Hyperlipid seems to think it was the small amounts of casein.

    2.Is it right to say that since the control carb meal only contained 174 calories compared to the butter meal which contained 800 this study is fairly useless? It raises some interesting questions but you can't conclude anything until you have a proper control containing the same amount of calories.

    3. Are there any studies which measure insulin secretion after a pure butter meal with no carbs?

    Even though the study is inconclusive, I'm lowering my butter consumption until I'm sure it isn't causing an agrovated insulin response. Even though butter causes much higher levels of FFA's which mean more of the fat is being burned, insulin levels that high can't be healthy

  • Miles

    3/20/2010 3:52:22 PM |

    All this information hurts my brain...ugh. All I know is when I eat low carb... I lose weight... feel better and more energetic. Sometimes there's just too much analysis and information about what constitutes a healthy diet. It's all opinion and based on research. Then other research refutes that idea.

    My Grandma used to say, "Eat when you're hungry and drink when you're dry."

    BTW... Grandma lived to be 95.

  • Helen

    3/20/2010 3:54:17 PM |

    Dr. Davis,

    I'm not too sure this is right.  I don't have the time to hunt down the links right now, but there was a study on Swedish children recently that showed those eating full-fat dairy (butter fat) were leaner than those who ate low-fat dairy.  Also, butter contains a lot of CLA, which is now being sold as a fat-loss supplement.  I can't parse this study on its own merits like Peter or Pyker (though I thank them for doing so), but I remain unconvinced.  

    I also agree with other posters about the in-vivo, long-term evidence of dairy-reliant cultures and their longevity.  

    Again, with so many cautions of what not to eat, I'd love to see a Dr. Davis-approved diet plan.  If I were just following all the Don'ts, I'd go crazy (and hungry).

  • Anonymous

    3/20/2010 5:39:12 PM |

    The palmitic acid content of the butter would probably trigger  insulin when there is an abundant source of glucose in a meal.  But, if you look at this post by Stephan you will see that the body stores dietary fats when there is a glucose source of energy available.  


    As the glucose is depleted the fat is released to be used as energy.  The graph in Stephan's post clearly shows the cycling that occurs in normal metabolism.

    The information Dr. Davis presented showed an insulin spike, not continual high levels of insulin that would inhibit the release of FA as an energy source.
    I believe it was Dr. Eades who recently posted about the constant exchange of fats in and out of storage, and the implication is that storage is only a problem when cells remain saturated with glucose.  The fat never comes out because it isn't needed.  In this scenario insulin resistance and fat storage is protective.


    My understanding of this subject is, by limiting carbs, especially the sugar surrogates that are refined grain products, you can keep the normal cycling of energy sources going.

    When everything is working right, your body signals hunger and satiety appropriately, and the body runs at an equilibrium level of energy intake and energy expenditure.

    I suspect that the FA composition of butter makes it available as an energy source sooner than the other FA's tested in the study.  Hence the higher insulin level.

    I don't see where a moderate amount of butter, when there is a limited or low availability of glucose sources will make you fat, expecially if you are VLC or on a ketogenic diet.  I can see where it could be a problem if you were eating 150 or more grams of carbs per day and have metabolic syndrome.  Then high levels of insulin would spike even higher prompting the liver to pump out more glucose, and the fat just has no where to go except into storage.

    Take your vitamin D3 to get your adiponectin levels up.  Take fish oil while limiting Omega-6's to normalize inflammatory responses. Limit carbs, and get the glucose-FA cycle working for you.

  • Nigel Kinbrum

    3/20/2010 6:19:20 PM |

    Eating carbs with butter produces a big insulin response because butter induces temporary insulin resistance (IR) which means that more insulin has to be secreted to get the same net effect. Looking at the blood glucose response, the net effect is the same. So stop panicking. The temporary IR lasts for only a few hours.

  • Gretchen

    3/20/2010 7:49:28 PM |

    "Fat, in general, does not make you fat. But butter makes you fat."

    If you based your conclusion on the graph in this study, all fats make you fat.

    Protein also stimulates insulin, so protein makes you fat.

    Carbs stimulate insulin, so carbs make you fat.

    Conclusion: Food makes you fat.

    It's known that fatty acids acutely stimulate insulin synthesis. With chronic exposure to fatty acids (as occurs in obesity), insulin synthesis is blunted.

    I've never understood the body's rationale for this, unless a sudden infusion of fat makes it think it had better store the fat for the future, but with chronic stimulation it figures it has enough.

    I don't know how ingested fat is related to fatty acids in the blood, whether or not this is linear.

    Whatever, it doesn't look to me as if butter is much different from the other fats, and as others have pointed out, the amounts used in this study (on top of about 44 g of carb, which I wouldn't call a low-carb meal) were enormous.

    The other odd thing is that usually fats slow down a carb-stimulated blood sugar peak, and they didn't in this study.

  • Neil

    3/20/2010 10:33:31 PM |

    This is what is considered 'butter' in the study you refer to above Dr Davis and ultimately what this study uses to prove its point:

    "The subjects then ingested, within 15 min, a fat-rich meal consisting of dietary fat [50 g/m2 body surface area of butter, refined olive oil (ROO), high-palmitic sunflower oil (HPSO) or a mixture of vegetable and fish oils (VEFO) along with a portion of plain pasta (30 g/m2 body surface area), one slice of brown bread, and one container of skim yogurt]."

    Yep, that would be my definition of 'butter' as well!

    If that pile of c**p didn't raise your insulin levels what would?

    In addition: "The average total energy provided by the meals was 800 kcal (10 kcal/kg), and the macronutrient profile was as follows: 72% fat, 22% carbohydrate, and 6% protein"

    Only 22% carbohydrate, no chance of that increasing insulin levels either I suppose!

    It has to be the 'butter'

  • Peter

    3/21/2010 12:02:51 AM |

    @Helen: I couldn't have said it any better myself. I too remain unconvinced.

    You get fat from pasta, bread and butter in combination? Not really groundbreaking work.

  • Peter

    3/21/2010 12:19:14 AM |

    @Helen: I found the study you are referring to I believe.

    "BMI correlated strongly to fat mass and leptin was the best marker of overweight and fat mass in 8-year-olds. Food choice was similar to that at 4 years of age. An intake of fat fish once a week was associated with higher serum concentrations of n-3 fatty acids. The intake of saturated fat and full fat milk were inversely associated with BMI."

    The study was made at the University of Gothenburg.


  • Sue

    3/21/2010 12:51:41 AM |

    I'm sorry Dr Davis but you really didn't analyse this study properly before jumping to conclusions.

  • Anonymous

    3/21/2010 2:24:49 AM |

    Just wondering if you had seen this recent study about higher levels of Vit D being associated with increased arterial calcification in the African American population: http://www.eurekalert.org/pub_releases/2010-03/wfub-vdl031110.php

  • Mike

    3/21/2010 3:44:28 AM |

    Looking at insulin alone can be very misleading. If glucagon is released along with the insulin ,as happens when eating protein, then the fat storing effects of insulin are negated.

    For low carbers, the study is meaningless as it was done with lots of carbs. I will continue to eat butter and cheese until I see a meaningful study that shows that they cause a real problem.


    3/21/2010 6:02:42 AM |

    Maybe DR Davis saw something on that "low carb cruise" that didn't sit well with him and he's rethinking certain principles?

  • W. Bacon

    3/21/2010 8:19:58 AM |

    Dr. Davis' goof is discussed here:


  • Anonymous

    3/21/2010 5:25:38 PM |

    No, Neil, the 'butter' was just butter. They didn't have "that pile of c**p" at one time: each item in the list was a separate meal & separate data point. Unfortunately, the wording of the paper is in places not very good.

  • Helen

    3/21/2010 8:28:26 PM |

    "Anonymous said...

    Just wondering if you had seen this recent study about higher levels of Vit D being associated with increased arterial calcification in the African American population: http://www.eurekalert.org/pub_releases/2010-03/wfub-vdl031110.php"

    I saw it, and was hoping to discuss it in the pro-D blogosphere.

    I have two ideas why this might be the case.

    (1)  Because people of African descent are adapted to live nearer the equator, where the sun is all you need for enough vitamin D, they may not be as adapted as Europeans to use dietary vitamin D (supplements being an analogue), which Europeans probably relied on during winter months.  Thus, too much supplemental vitamin D may be harmful to African Americans, at least in the case of arterial calcification.  (I hedge, because I've also read recently that African American children with low D status have higher rates of asthma. http://www.sciencedaily.com/releases/2010/03/100317112055.htm)

    (2) There is also the possibility that somewhat different dietary patterns between European Americans and African Americans may offer some explanation.  I can't imagine what this might be, but maybe something having to do with vitamin K2, which helps prevent calcium deposits in the arteries?  There are two possibilities here:

    (a) Maybe African Americans consume (or produce in the gut - from eating greens, a traditional part of the African American diet) more K2 than European Americans, and this is why they have less arterial calcification with lower D status - they don't need the D as much for arterial health, and more dietary D just upsets the balance.

    (b) Maybe they eat less K2 than European Americans (maybe eat less hard cheeses?), and thus vitamin D supplementation, which may require a certain level of K2 to be beneficial, might be harmful instead.

    This sentence leads me to believe it's more likely to be (a):  "Despite these lower vitamin D levels and dietary calcium ingestion, blacks naturally experience lower rates of osteoporosis and have far less calcium in their arteries."  The strong bones and clear arteries make me think African Americans may have better K2 status.  

    It's possible that vitamin A status also plays a role.

  • Helen

    3/21/2010 8:56:30 PM |

    Another thought on the question of African Americans and vitamin D - perhaps *because* they consumed less calcium their vitamin D requirements were lower, so the supplemented amounts were excessive.

  • Dr. William Davis

    3/21/2010 9:55:55 PM |

    The point is not whether glucagon is stimulated. That is, in my view, immaterial.

    The point is that your poor, tired pancreas, likely operating at a fraction of its original beta cell capacity from the years of the beating it took while you ate Cheerios and Cocoa puffs, ate sandwiches, and drank Coca Cola with your pizza, is being stimulated to produce more insulin.

  • Nigel Kinbrum

    3/22/2010 9:05:25 AM |

    Regarding calcification, I think that Helen has hit the nail well & truly on the head regarding Vitamin K2. "If it calcifies, think K2" is what I always say (along with "If it spasms, think Magnesium").

    Taking large amounts of Vitamin D3 and nothing else probably exposes deficiencies in the other fat-soluble vitamins A, E & K2.

    Having cured Lumbar osteoporosis in three years using Ca, Mg, D3 & K2 (and no Alendronate), I will never stop taking Ca, Mg, D3 & K2.

  • Anonymous

    3/22/2010 8:15:10 PM |

    Why eat carbs together with fat?
    They ate 44 g glucose which means the P-glucose could reach >48 mM without insulin i 70 kg person. Of course the disaster hormone insulin increases to block all lipolysis as well as proteinolysis to try to burn off all the totally unnecessary carbohydrates they added.
    If contol diet (gluose) did not change glucose and thus insulin level it must be fake.

    Just another totally stupid study.

  • Anonymous

    3/22/2010 8:53:10 PM |

    I guess I am going to become a breatharian....someone who survives only on air.....since I have learned that butter and fat stimulates my insulin, protein stimulates my insulin, carbs stimulate my insulin and thus I am doomed to be fat....and leptin is stimulated by all three but my brain doesn't register that I am full.  

    Ingesting air is the only thing that will not make me fat.

    Go here to be a Breathairian http://www.breatharian.com
    You can even go to a $1 million dollar seminar that must be completed prior to Dec 21, 2012.

  • Dana Seilhan

    3/22/2010 10:20:44 PM |

    When I'm low-carbing, a favorite meal is a tenderloin cooked medium-rare, sliced thin, and dipped in butter.

    I lose weight anyway.

    Also, what kind of butter was used in the study?  Was it regular grocery-store butter, or was it organic and/or grass-fed butter?  The FDA claims there's no difference between dairy produced with rBGH and dairy produced without, but I'm given to understand that rBGH-produced dairy has higher levels of IGF-1.  What would be the effect on insulin of all that exposure to insulinlike growth factor?

    And I'll second Miki's question of whether the milk solids wouldn't make a difference.

    And to the person who mentioned "all that lactose-y yogurt"--if you make yogurt correctly, it should have hardly any lactose in it at all.

  • Dana Seilhan

    3/22/2010 10:22:01 PM |

    I suspect that the FA composition of butter makes it available as an energy source sooner than the other FA's tested in the study. Hence the higher insulin level.

    Fatty acids by themselves don't prompt insulin release.  Protein does (but the insulin is balanced out by glucagon), and of course carbs do, but there's nothing inherently dangerous in a fatty acid that would prompt the body to store it away immediately.

  • Anonymous

    3/23/2010 7:02:21 PM |

    It seems like no one has a handle on how the metabolic parts fit together to make the whole. My experience from converting from whole grains and no-fat dairy to full-fat dairy has been weight loss and increased energy, particularly after eating a selection of artisan cheese. I often get up, have a bowl of full-fat yoghurt or kefir with 100% chocolate nibs and fresh-roasted nuts, then sample several artisan cheeses, and go cycling 44 km before getting back to make everyone else breakfast. My body seems geared to fat as fuel and I never get blood sugar lows. If this is raising my insulin, it apparently does not affect my blood sugar.


  • Apolloswabbie

    3/25/2010 7:38:15 PM |

    Usually, I learn all I need to from Dr. Davis' posts.  My thanks to the other contributors today for illustrating that context is everything.  We have reason to believe that dairy from the industrial food chain would not be as good a food as if we could get true grass fed dairy cow products - but this seems out of context with other info I've seen which shows only moderate insulin response to dairy fats.  Bottom line: measure the markers which indicate insulin levels over time as a gauge of whether your diet does/doesn't work (unless you are losing weight - in which case, you know it is working).

  • Anna Delin

    3/26/2010 9:42:22 AM |

    It seems that whatever butter does to my insulin levels, this does not curb the very positive effects I experience from eating butter. When I cut carbs and replaced them with generous amounts of cream and butter (organic preferably) I lost 14 kg. Moreover, when in "carb country", i.e. airports, airplanes, trains and the like, I can keep my energy up by eating the small amounts of butter and cheese available. Butter also has a way of keeping me feeling full for a very long time. This implies that the fat is not stored away in my fat cells but instead made available for burning. Perhaps other people are more sensitive.

  • ET

    3/26/2010 11:46:15 AM |

    While I often disagree with the conclusions you post, I always enjoy the discussions and research raised by your blogs.  It's one reason I keep coming back for more.  It's keeps me searching for answers.

  • Star Trek TNG

    3/28/2010 6:13:00 PM |

    I still prefer coconut oil for fat loss used in a no-carb diet. I'll find that ghee, which I've also tried, isn't so effective for weight-loss perhaps because it's not so fatty. But it does have to be in a no-carb diet, not a low-carb one. Everyone's got a switch which is triggered by carbs, but no-one knows where it is, not exactly. So unless a study is rabidly no-carbs, none at all, I don't really see what can be learned.


  • Nancy

    4/8/2010 12:53:02 AM |

    Dr William
    your response to the commentors seems to indicate that butter will make you fat IF you have abused your body with carbohydrates because of a compromised pancreas.  I am willing to suppose this could be true, but what about people who his ave not abused their bodies, what about children being raised low carb from the start, would butter be fattening for them?  Your response would lead me to believe your answer will be no.  I really appreciate your blog and recommend it to all, but please clarify this issue.  Maybe a whole new blog on this would be a good idea, since the entire low carb community is talking about it.

    To everyone else I have to say there is nothing like testing something for yourself.  If you have an insulin tester, have some butter and test yourself and make a chart.  See how YOU are affected.

  • Alejo Hausner

    4/9/2010 1:28:50 PM |

    The work was funded by the Fundación Centro de Excelencia en Investigación sobre Aceite de Oliva y Salud (“Center of excellence for research on olive oil and health”).

    Notice that they end up concluding that olive oil raised glucose and insulin less than butter. Had this study been done by French researchers and not Spanish researchers, it would have found that butter is better for you than olive oil!


  • jpatti

    5/7/2010 7:58:00 AM |

    Pasture-raised butter is a good source of vitamins A, D and K2 plus CLA.

    And it makes veggies yummy.  

    As Julia Child said... butter is better.

  • info

    5/16/2010 6:10:09 AM |

    Little test
    I'm a very low carber. 80% of my calory intake come from fat. I eat less than 20 grams of carbs. I did a little test. For a week I took tallow and coconut oil instead of butter. In that week I lost three pounds. Conclusion: Butter seem to have a sort of effect.

  • kimberly

    9/16/2010 1:46:12 AM |

    I love to prepare some recipe that contain many cream.  although i know that a person can gain weight I don´t matter because i love the taste, Simply delicous. And when i cook, my husband usually is very happy.
    Actually i was looking information about how tobuy viagra  but i reached this blog, i really enjoyed reading.

  • buy jeans

    11/2/2010 8:24:56 PM |

    The postprandial (after-eating) area-under-the-curve is substantially greater when butter is included in the mixed composition meal. This effect is not unique to butter, but is shared by most other dairy products.

  • Chester The Bear

    1/19/2011 10:55:45 PM |

    Um... Sorry... I see the data differently.
    In the fat meals in the study, the amount of fat intake was the same, yet butter delivers higher serum FFAs, indicating that fat might stimulate lipolysis, even though it appears to induce a short term insulin spike.
    Carbohydrate might promote a lower insulin response, but it blocks lipolysis.
    Finally, there's a lot more going on here than just insulin.  To take it out of context is meaningless.

  • racing games

    1/20/2011 11:15:13 AM |

    but my question is what is the reason behind this insulin triggering effect of butter? can anyone answer this?

  • liposculpture guide

    1/26/2011 7:18:57 AM |

    It's always good to challenge deeply held beliefs in case we are wrong. I do have a soft spot for butter and hope it is an outlier as far as blood glucose.

  • francisco camps

    2/5/2011 8:41:02 PM |

    I am scary with butter now...lol


    3/5/2011 6:27:47 AM |

    As people know, I've been struggling with my weight due to my hypothyroidism. Although many of my symptoms have improved, I kept the weight gain in very consistent rate of 3 pounds per month. Sometimes, mostly due to a little fast, would be a pound or two, but then suddenly I would like to recover all that weight plus more than a day or two, so it would be in this constant uphill again.

    people searches

  • Matt Titus

    5/6/2011 3:42:50 AM |

    I wonder if the results would be the same with raw butter?

  • Paula Nedved

    10/3/2011 2:30:40 AM |

    Peter over at Hyperlipid has done a critique of this post of your, Dr. Davis.
    Entitled "Butter insulin and Dr. Davis"    He dunna believe you.

  • Nancy

    10/20/2011 4:57:58 PM |

    I'm stunned by your absolute condemnation of butter based on this one study.  Geez, have you been paid off by Wesson or Crisco?   You need to consider all the confounding variables in this study.  Your blog post should be retracted and/or rewritten.  This is very disappointing after your carefully researched examination of wheat.

    In my experience, butter and butter fat are good for you.  I have lost considerable body fat and gained much muscle this year on an eating plan that involves a lot of raw milk and cream from grass-fed cows, 3 to 4 glasses of milk and up to a cup of cream per day.  Butter fat is not making ME fat, quite the opposite.

  • Karl Schmidt

    9/27/2012 6:35:46 PM |

    Insulin goes down faster because the vegetable fats are stored in the fat tissue faster..

    A better understanding of butter is here :


  • Karl Schmidt

    12/1/2012 9:41:46 PM |

    There is another problem with that study - people do not keto adapt in 8 hours - it takes 4- 6 weeks to fully adapt to a low carb diet.

    Once adapted, low-carbers are BETTER able to clear FA as the liver revs up it's fat metabolic capabilities.  Low carbers also tend to eat less frequently - reducing the exposure to both BG and FA - only when both are elevated do we see the pronounced toxic effects of the fats.

HDL 80 mg/dl

HDL 80 mg/dl

More and more people in my clinic are showing HDL cholesterol values of 80 mg/dl or higher, males included.

Think about it: Nationwide, average HDL for males is 42 mg/dl and for females 52 mg/dl. Even though these average values are generally regarded as favorable, HDL cholesterol values at these levels are nearly always associated with higher levels of triglycerides, postprandial (after-eating) lipoprotein abnormalities, and excessive quantities of small LDL particles.

HDL particles are, of course, protective and are powerfully anti-oxidative. Higher levels of HDL have been associated with reduced potential for cancer, as well as reduced risk for heart disease.

Following the simple regimen that we follow to gain control over coronary plaque has therefore increased levels of HDL to heights that are uncommon in the rest of the population, levels that readily top 80, 90, or 100 mg/dl. That regimen includes:

1) Elimination of all wheat--Yes, consumption of "healthy whole grains" sets you up to have lower HDL levels; elimination of wheat increases HDL.
2) Limited carbohydrate consumption--While eliminating wheat is a powerful nutritional strategy to increase HDL, non-wheat carbohydrates like quinoa, millet, beans, rice, and fruit can still cause high triglycerides that lead to reduced levels of HDL. Limited exposure helps keep HDL at higher levels.
3) Omega-3 fatty acid supplementation--Because omega-3 fatty acids reduce both triglycerides and blunt the postprandial rise in lipoproteins that can cause HDL degradation, HDL rises with omega-3s from fish oil.
4) Vitamin D supplementation--The effect is slow, but it is BIG. HDL just goes up and up and up over about 2 years of supplementation. Before vitamin D, HDL levels of 60 mg/dl were the best I could hope for in most people. Now 80 mg/dl is an everyday occurrence.

Other factors can also be used to increase HDL levels, such as weight loss, red wine and alcohol, exercise, cocoa flavonoids, green tea, and niacin. But following the regimen above sends HDL through the roof in the majority.

Comments (73) -

  • Kurt

    11/14/2011 1:46:29 PM |

    I have had a similar result. I eliminated most grains except brown rice, I take one Fisol fish oil capsule with each meal and 1,000 iu of Vitamin D each day. My most recent HDL reading was 79 mg/dl, up from 63 mg/dl about 18 months ago, and 15% higher than my highest reading ever. I was pretty pleased.

  • majkinetor

    11/14/2011 2:49:33 PM |

    What is your opinion on high HDL + high [hs]CRP. Some doctors understand this as marker of inflammation or auto-immune disease.

  • Melissa

    11/14/2011 2:50:04 PM |

    I'll share some (half) of my HDLs with the highest bidder. I worry about mine being too high (they've always been ridiculously high). Is there ever a tipping point where high HDLs are an indication of inflammation? BTW, for the most part, I've been on the regimen you mention above for ages. I've never taken niacin and I don't drink alcohol other than occasional red wine, but I get lots of exercise in the form of yoga, hiking, skiing, etc. I never step foot in a gym. =) I've been GF for a decade.
    Hope all is well with you!

  • Fat Guy Weight Loss

    11/14/2011 3:01:30 PM |

    Sounds like I am doing everything right.  Looking forward to my next cholesterol test to see how high my HDLs are.  So what is your recommendation for Vitamin D supplementation?

  • Linda

    11/14/2011 3:25:04 PM |

    Yup, I am doing all these things recommended by our "esteemed leader" and I am proud to say that my most recent blood work indicated Triglycerides at 49 and HDL's at 90!!!
    Have to see a cardiologist this week due to some weird chest pressure a week ago, no "cardiac event", just weird pressure,  which brought about an angiogram and a stent insertion. I am braced for the inevitable "statin lecture" which I have already endured while still in the hospital. If he persists in pushing this drug, I am going to walk out of his office and look for another doctor.
    With a Tri/HDL ratio of .54, there is no way I am going to swallow statins everyday, destroy my liver and/or muscles, and end up buying more #%*$%  drugs!

  • Kenneth

    11/14/2011 3:41:53 PM |

    Is this fabled HDL effect of Vitamin D somewhat linear over the initial two years or is it some sort of tipping point effect where your HDL jumps up sharply after some sort of saturation point?  Over 8 months or so this year I got my D levels up from about 30 to 60. During that time, my HDL actually dropped from mid to low 30s!  My TG levels are rotten at about 300 even with lots of fish oil and a gram of Niacin.  I've also cut back considerably on carbs, though going wheat free is a real struggle for me.  Is a D-25 level of 60 high enough to see a potential HDL boost? Does one have to wait a full two years to know if you're going to be a responder or not? I've resisted the idea of statins or tricor for years, but I'm not getting a lot of traction with the alternatives. At what point is it reasonable to "throw in the towel"?

  • James Winningham

    11/14/2011 6:42:00 PM |

    Dr. Davis,

    Good information on Omega 3s. I remember reading a lot about the ratio of Omega 3s to 6s, and that Flax oil had that correct ratio. Is there anything to this?

  • Jonathan Carey

    11/14/2011 7:23:06 PM |

    Even with familial hypercholesterolemia, I tripled mine from 34 to 91.  My non-commercial website tells how I did it.

  • Might-o'chondri-AL

    11/14/2011 7:53:41 PM |

    Hi Kenneth,
    If Doc's protocol , & not just recommended supplements but his insistence on carb control, is not producing the anticipated adult trig results then autophagy is likely problematic. Triglyceride (trig) breakdown is less when one's capacity for auto-phagy (cellular self cleaning) is less. The Korean Healthy Twin 2008 study sets trig heritability as +/- 46% but did not parse the genetics.

    Genetics of the autophagy related gene 7 (Atg) means that an individual with low Atg 7 will have less autophagy in the liver and more trigs hanging around in the liver since their liver trigs are not being broken down quickly. And yet, in the young especially,  contrary to linear logic less autophagy "normally" fortuitously trends toward less trigs in the adipose (fat) tissue. So, even a non-obese adult with relatively less adipose mass there can be a genetic quirk inciting high trigs coming out from the liver into circulation that doesn't readily seem related to diet.

    Inside each cell is an auto-phagosome component that is designed with it's own dual membrane to hold lipid "droplets". It is from hydrolysis of trigs in lipid droplets that the liver gets the trigs it sends out from the liver with VLD - this is the trig rich VLDL shuttling which Doc warns us  fosters smLDL.

    The auto-phagosome (cell's self scavenger) is the cellular component that 1st has to be able to pick up the lipid droplet and then move on over to the lyso-some organelle inside that same cell to conjoin. Only then can the un-needed trig, that is now inside the lyso-some, be degraded by the cell's natural lyso-some action. For most aging/old individuals their liver autophagy capability declines and so their livers risk the burden of piling up lipids; &  that can contribute to the age associated progression of the metabolic syndrome's high trigs.

    Doc would know better than me the clinical worth of O'Keefe's  2009 Mayo Clinic symposium contention that  EPA/DHA of 3-4 grams daily is useful to lower trigs, whereas  common 1g/d dose is beneficial against human endothelial/arterial dysfunction. The omega-3 EPA lowers the trigs more than the DHA molecule.

  • Ensues

    11/14/2011 8:32:52 PM |

    I wish I could experience the HDL rise I consistently read about.  I am convinced I have familial hypertriglyeridemia.  I do not eat wheat, supplement aggressively with Vitamin D, and take a significant amount of Pharmx liquid fish oil daily and I cannot achieve an HDL marker above 24.  It ran 23-24 before all of the other actions.  It just does not move despite the interventions.   Starting to titrate up on Niacin now.  Will try everything before I capitulate to a fibrate.  If I lived in WI I would be making an appt with Dr Davis!

  • Bill

    11/14/2011 10:03:33 PM |

    My HDL is off the chart at 159. It's so unusually high that my doc has no idea whether it's good or bad, or what it means.

    He says it's 50% higher than the next highest he's ever seen. He had a hard time thinking of *any* lab result he's seen from any patient that was 50% higher or lower than the max or min he's ever seen in others in his many years of practice. He thinks it definitely means something big, but what?

    He suspects either a genetic oddity (my mother's HDL has always run quite high, too, though not nearly that high), a chronic, latent infection, or ominous autoimmune problems beyond my known Hashimoto's.

    He does not know if my HDL of 159 means my (calculated) LDL of 217 and impressive total cholesterol of 382 are safe or not. My triglycerides are an impeccable 39.

    I plan to do full lipoprotein panel at some point to clarify these strange numbers. I really don't know whether to celebrate or worry. I'm not sure anyone has the answer.

  • Kenneth

    11/14/2011 11:49:40 PM |

    If someone can figure out how to separate out some of your sky-high HDL with plasmaphoresis and preserve it as a blood product for re-infusion, some of us could take some of it off your hands! Smile

  • steve

    11/15/2011 12:14:00 AM |

    Nice to hear about the HDL improvements, but what about particle count? No doubt small LDL particles may decrease, but how high is everyone seeing there Large LDL particles increase to?  It also may be unclear that higher HDL is in and of itself beneficial; many with high HDL have ever increasing calcium scores.

  • Might-o'chondri-AL

    11/15/2011 2:30:30 AM |

    Hi Majknetor,
    CRP (C reative protein) level is more significant regarding the stabiity of plaque (ie: risk of rupture) and less indicative of  the degree of coronary artery calcification.  CRP  can be a marker for other physiological doings in non-cardio vascular pathological processes an individual is undergoing. When adjusted for age and race relying of  CRP as a predictor of heart problems is not precise.

  • Might-o'chondri-AL

    11/15/2011 2:54:23 AM |

    Hi Ensues,
    Lancet's U.K. 2010 meta-analysis ("Effect of fibrate on cardiovascular outcomes: a systemic review & meta-analysis") indicates that fibrates for those with low HDL & high trigs are preventative in the context of  suffering less coronary disease and less re-vascularization surgery  being needed. But,  that  fibrates have no  beneficial effect on strokes  (since strokes, whether hemorhagic or embolism is not "driven" by cholesterol in plaque). And,  in terms of  amount of cardio-vascular fatal events fibrates offer no statistical benefit  vs. not taking fibrates when look at  how many actually die from cardiovascular events.

  • Might-o'chondri-AL

    11/15/2011 4:39:11 AM |

    Unsolicited low HDL primer:
    HDL has protein (ApoA1 & ApoA2) & lipids (cholesterol esters, triglycerides, sphingomyelins & glycerophospholids). "Normally" +/- 70% of  HDL protein is ApoA1 & +/-20% is ApoA2. If your genetics stick you with reduced ApoA1 then that contributes to low HDL levels &  generally ApoA2 is less affected by genetics.

    When % of trig burden in HDL goes up & it  gets to the kidneys that  trig rich HDL's ApoA1 protein undergoes endo-cytosis (engulfing) and the ApoA1 is cleared away by the kidney (whereas ApoA2 is not excreted by the kidney). Then, in this trig dynamic,  HDL levels stay low - since person is repeatedly shy of ApoA1 to build with. If there is genetic low ApoA1 to begin with then this further limits the elaboration of HDL; especially considering ApoA1 is broken down (& eliminated) faster than ApoA2 anyway.

    Mass spectrometry analysis shows high HDL is most notably associated with  high sphignomyelin levels - since a feature of  high HDL is less trigs  and usually cholesterol esters are only 13 - 27% of the lipid particles on HDL  the it's sphingomyelin carrying capacity goes up . The ApoA2 protein has more affinity for trigs (& cholesterol esters) since ApoA2 limits the other lipids ability to get on the HDL surface; so it is easier to have higher sphignomyelin when there is less Apo2 in one's HDL .  The more ApoA2 , at the expense of ApoA1, the more trigs and more VLDL (fibrates work, in part,  by acting on Apo2's gene regulatory element).

    There are gender differences in HDL levels.  The Dutch Erasmus  Rucphen study puts HDL heritability at 54%  & Caucasians seem more prone to low HDL than some other stock..

  • Might-o'chondri-AL

    11/15/2011 8:52:15 AM |

    cont. (in case some didn't know relevance):
    Having high amounts of HDL means there is lots of sphingomyelin tied up by HDL's ApoA  & thus less freely circulating sphingomyelin to get picked by LDL's ApoB . Blood plasma levels of sphingomyelin are associated with coronary artery disease all by themselves, as a stand alone marker without being referenced to one's cholesterol level.

    This relates to HDL's potential to limit the progression of atherosclerosis &  not HDL's well touted role in reverse cholesterol transport .  When small LDL's ApoB  lipoprotein with a burden of sphingomyelin gets into an artery wall the enzyme sphingomyelinase can hydrolizes  it in a way that leads  to that ApoB's aggregation. Then that lipoprotein can't readily get back out &  it stays there in a form that  adds to the polymerization which occurs when the macrophage foam cell it is in dies and incorporates into plaque.

  • Alexandra

    11/15/2011 11:09:31 AM |

    I haven't ever had complete bloodwork done...well, 18 years ago when I was pregnant with my final child, they took what seemed like a quart of blood from me but those results were never mentioned to me, so I don't know what was done.  If I find a doctor and ask to have bloodwork / a lipid panel, etc. done, what should I ask for? Is there a specific wording required on the prescription so that the lab will check for small vs fluffy?  Vit. D levels, etc.  What else should be checked?  I am 50, have never been ill beyond a cough or cold.. I check my own BP, avg about 118/78. I test my own BS...fasting is in the 80's.  I've been low carb for 4 years (lost 120+lbs) and LC paleo for over 1 year. I feel better than ever so maybe its time for bloodwork to see if things are going as well as I feel they are.
    I appreciate any suggestions.

  • Dr. William Davis

    11/15/2011 1:08:21 PM |

    Hi, Alexandra--

    Ask for lipoprotein analysis. I prefer NMR lipoprotein analysis. However, if your doctor gives you a blank stare, it's not time for asking for labs, but time for a new doctor.

  • Dr. William Davis

    11/15/2011 1:11:42 PM |

    HI, Bill--

    The whole notion of HDL functionality, i.e., separating good from bad effects, is still in its infancy. And, yes, the HDL without doubt increases total cholesterol. Yet another reason why we should completely discard lipid values and only use lipoproteins. My bet is that your measured LDL (e.g., NMR LDL particle number or apo B) are far lower than the calculated value would suggest.

  • Dr. William Davis

    11/15/2011 1:13:47 PM |

    Hi, James-

    Imagine seeing you here!

    Flaxseed is a great source of linolenic acid as an omega-3; it may have modest independent benefits outside of conversion to DHA/EPA. Chia likewise.

  • Dr. William Davis

    11/15/2011 1:14:51 PM |

    Yes, it's likely something close to linear.

    Also, note that, if your diet results in weight loss, there will be a transient DROP in HDL, only to be followed by a long, slow rebound.

  • Dr. William Davis

    11/15/2011 1:15:47 PM |

    Also, Linda, look for other factors, such as Lipoprotein(a), vitamin D deficiency, thyroid dysfunction.

  • Dr. William Davis

    11/15/2011 1:16:16 PM |

    Sufficient to achieve a 25-hydroxy vitamin D level of 60-70 ng/ml. Please see the 3 million posts on this blog about this.

  • Dr. William Davis

    11/15/2011 1:18:01 PM |

    Hi, Melissa--

    The data on the potential inflammation and other counterproductive functions on HDL are still too early for prime time. So right now we have measures like total HDL, apo A1, HDL particle number and large vs small HDL. Boston HeartLabs has some additional measures, but I still do not know now valid these measures are. I'd also like to see better corroboration of the French groups indictment of inflammatory HDL before we start to pursue this avenue.

  • Dr. William Davis

    11/15/2011 1:18:49 PM |

    Never heard that.

    I see CRP as a marker of wheat and carbohydrate consumption, along with vitamin D deficiency. Correct those two and CRP almost always drops to zero or close to it.

  • Linda

    11/15/2011 2:35:05 PM |

    Vitamin D3 supplementation?  Check
    Thyroid dysfunction?   Blood test done. TSH was 2.70. Early AM temps are always below 97.8 but my doctor does not see a problem.

    Lipoproteins?  They don't bother to check for that, guess they don't see the importance, at least among the doctors I've seen.

    Oh well..........................

  • berger6696

    11/15/2011 5:05:14 PM |

    I've been wheat free vlc paleo for 6 months.  I've also been supping with 3 1000 mg fish oil and 4000 iu vit D daily for the past 3 months.  My HDL has fluctuated but basically stayed in the mid/low 30's, while my total, LDL and TGs have gone up significantly.  What do you make of this?

  • Alexandra

    11/16/2011 1:20:00 AM |

    Thanks... I don't have a doctor so that will help me weed them out a little.

  • Ensues

    11/16/2011 5:53:30 PM |

    Thanks for the comments Al!  There lies the dilemma I have struggled with.  Do I medicate just to chase a marker?  Looks like some benefit in terms of disease reduction but is that worth any negative consequences from the medication?  I really wish the data was more definitive.

  • Ensues

    11/16/2011 5:54:45 PM |

    No.  BMI hovers around 32-33 after a year of paleo template eating.  (Lost 25ish lbs)

  • Might-o'chondri-AL

    11/16/2011 6:11:56 PM |

    Hi Alexandra ,
    Like you I have no USA doctor , so for NMR twice used (what is now called) iNeedLabs.com : an online service - no prescription required; pay for  tests prior to visiting your local blood draw lab... their doctor authorizes blood draw (not available in N.Y./N.J../Mass./R.I.)

  • Linda

    11/17/2011 12:39:03 AM |

    Dr, some questions for you?
    1. Are statins ever helpful?
    2. Once you take them, are you on them forever?
    3. I now have one stent after an angiogram detected blockage. I also have blockage in two other areas. Is it necessary for me to take a statin even with an excellent HDL/triglyceride ratio, etc?
    4. Dr. tells me if I refuse statins, I WILL have a heart attack!
    5. I am female, over 60, following LC diet, taking D3 5000 IU, etc.

    I have not had a cardiac event, simply chest pressure.

  • Dr. William Davis

    11/17/2011 1:05:10 AM |


    I invite you to read the 1100 posts preceding this one. Note that this blog will not replace your doctor, just help you be better informed.

  • Dr. William Davis

    11/17/2011 1:06:18 AM |

    Insufficient information, Berger.
    If weight loss has occurred, for instance, triglycerides will go up, HDL will go down, LDL can do anything. This all improves when weight plateaus.

  • majkinetor

    11/17/2011 9:54:34 AM |

    There is some info about it here:

  • majkinetor

    11/17/2011 9:58:24 AM |

    Do you think that IF style eating trains autophagy pathways ?

  • berger6696

    11/17/2011 12:58:26 PM |

    Thanks for the reply Doc!  I'm 5'9.5 135lbs.  Vary low body fat and pretty athletic build.  I crossfit.  When I started paleo I was 145 with much more fat around the waist (I swim in my old pants, lost about 2-3" around waist).  I feel really good but my labs are just not working with me (I sent you a copy of my VAP test on Fbook).  I'm just really confused on why my labs are not doing what they should and what to try next?

  • Might-o'chondri-AL

    11/17/2011 9:16:53 PM |

    Hi Majkinetor,
    You're concerned about high HDL & linked to it's relationship with inflammation. Virus (& some bacteria), whether symptomatic or not,  want to use sphingomyelin (HDL carries some) because a series of enzymes converts it into sphingosine-1-phosphate (S1P;  HDL carries some S1P). In some cases super high HDL may be attempt to short out a virus (ie: remove circulating sphingomyelin substrate & clear S1P away)  while the more ancient  viral adaptability tries to take advantage of the situation.  Pathology  worsens when viral proteins "lay" on lipids blocking the micro-somal tri-glyceride transfer protein from promoting key lipoprotein events (beneficial ApoB/VLDL /trig dynamics) in the liver cells' endoplasmic reticulum; & also viral proteins "goop" on to ApoA1 (HDL's main protein) in the golgi apparatus.

    The S1P works both inside and outside cells in "normal" health as a signaling molecule. Viruses (& cancer cells) contrive to hijack this dynamic for those signal effects on cell motility (scoot over), cell's ability to survive challenges, proliferation of cells and in some inflammatory processes. S1P can alter the Calcium 2+ level inside a cell  to put into play enzymes that foster th inflammatory cascades (ex: inside cell cytolsolic phospholipase A2 enzyme being set off makes Arachidonic acid get free to make inflammatory leukotrienes, prostaglandins & thromboxanes - which, many recognize are also unwanted agitators of cardio-vascular inflammation). When the S1P lipase enzyme is around then it breaks down S1P (cancer  blocks S1P lipase enzyme, because without S1P cancer goes apoptotic/dead).

  • Ryan

    11/17/2011 9:35:47 PM |

    US News ranks diets.  Here is what they said about Paelo and no Grains...

    "Possibly. By shunning dairy and grains, you’re at risk of missing out on a lot of nutrients. Also, if you’re not careful about making lean meat choices, you’ll quickly ratchet up your risk for heart problems." -- So you are missing out on a lot of nutrients... then they don't name any nutrients you would be missing.  So they are really trying to say if you eat a lot of different veggies and fruit and lean meats and nuts, etc... I would be missing out on something grain offered?  

    Grains vs other food groups: http://robbwolf.com/book-resources/

  • Kenneth

    11/17/2011 11:50:08 PM |

    Much has been written here about statins and their relative benefits and limitations. Does anyone have any thought/experiences to share about fibrates, specifically fenofibrate? After years of inadequate progress on my triglycerides by other means, I'm going to give generic tricor a shot. My doc doesn't seem to think statins would be of much help with TG, with the possible exception of lipitor, which would be an insurance nightmare.  I can't seem to find a lot of "street wisdom" about Tricor or that class of drugs. It seems to have sort of a nasty reputation for side effects - GI upset and a relatively high incidence of liver trouble.  On the other hand, the potent statins and doses required to really dent TGs would have their own issues too?

      Are there any dosing strategies or nutrients which might mitigate side effects of fibrates  the way Q-10 can with statins?  I'm a bit nervous about taking this plunge into such pharms, but I'm not getting where I need to be with diet, fish oil, niacin and Vitamin D.  I've tried other things touted for this like Sytrinol to no effect. I just don't see a lot of "low-hanging fruit" solutions left. I'm not diabetic, not more than maybe 7 pounds overweight. I'm going to get evaluated for thyroid in a few weeks and that could turn out to be part of it, but in the meantime I've got a script for fenofibrate with my name on it....

  • Linda

    11/18/2011 12:34:00 AM |

    Dr. Davis this information was given on the "Morning Joe" program on MSNBC  11/17/11 what can we get out of it?By Linda Carroll
    msnbc.com contributor
    updated 11/16/2011 3:50:04 PM ET 2011-11-16T20:50:04
    Print Font: +-When it comes to the heart, vitamin D can be a double-edged sword.

    Scientists have long known that low levels of the nutrient can hurt the heart, but new research shows that higher than normal levels can make it beat too fast and out of rhythm, a condition called atrial fibrillation, according to a report presented at the annual meeting of the American Heart Association.

    The study, which followed 132,000 patients at a Utah based medical center, found that the risk of newly developed atrial fibrillation jumped almost three-fold when blood levels of vitamin D were high.

    Most people get at least some of their daily needs of vitamin D from sunlight. But in cold northern climates where everyone bundles up for the winter -- inadvertently blocking rays that raise the body’s vitamin D levels  -- people are often encouraged to take supplements to boost levels of the nutrient to protect the bones and heart, said the study’s lead author, Dr. Jared Bunch, director of electrophysiology research at the Intermountain Medical Center in Murray, Utah.

    However, because everyone absorbs these supplements differently, blood levels need to be tested to make sure they’re in the safe range, Bunch explained.

    High levels of vitamin D only occur when people take supplements, Bunch said. Because consumers assume supplements sold over the counter are safe, they may not realize the danger of taking too much vitamin D, he added.

    “People are looking toward therapies considered to be natural to treat a broad variety of disease states and as a means of prevention,” Bunch said. “We see patients who take a tremendous amount of vitamin supplements.”

    Advertise | AdChoicesAdvertise | AdChoices
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    .Bunch said the normal range for vitamin D was 41 to 80 nanograms per deciliter (ng/dl). Patients in the study were designated as having excessive vitamin D had had readings above 100 ng/dl.

    The recommended daily intake of vitamin D for people from 1 year to age 70 is 600 IUs, or international units a day, based on what is sufficient for bone health, according to the National Institutes of Health. There are few natural food sources of vitamin D, although oily fish such as tuna or salmon are among the best. For example, 3 ounces of cooked salmon contains 447 IUs of vitamin D per serving. Small amounts are also found in cheese and egg yolks. The Department of Agriculture provides a comprehensive list of foods containing vitamin D.

    Bunch advised people who have recently been diagnosed with atrial fibrillation and are taking vitamin D supplements to make sure their doctors check blood levels of the nutrient.

    He suspects that the effects of high vitamin D on heart rhythms are reversible.

    “If the levels are excessive, I would hope that when they’re cut back the arrhythmias would improve as well,” Bunch said.

  • Alexandra

    11/18/2011 1:52:49 AM |

    Thanks,  I happen to be in rural NY...

  • Might-o'chondri-AL

    11/18/2011 2:49:36 AM |

    Again Majkinetor,
    Cell's internal proteo-some takes misread/misfolded/worn out proteins (including nitrated MnSOD) apart  via proteo-lysis for recycling the amino acids, since aminos too "costly" to just ditch & cell wants to control it's  protein concentration in real time. Cell's lyso-some in the old person have less portals to get the damaged mitochondria & lipid droplets in for recycling so usually the aged have 10- 20 %  "cluttered up" cells (ex: neurofibril tangles in Alzheimers uses junked mitochondria membrane segments that collapsed). TFEB is the master protein that switches on our lysosome building gene & thus helps improve autophagy play out.

    A low calorie dieter performs pretty robust  autophagy so is potentially less disease prone & that liver is not burdened with so many defective molecules. However, full-on calorie restriction sees reduced autophagy - probably (?) because most everything molecular is crucially needed right where it is ("if it ain't broke don't fix it" paradigm). Intermittent fasting is like periodic starvation and is a type of full-on calorie restriction; so extended fasting inhibits autophagy.  This it should be pointed out is different (nothings simply linear) than when we normally overnight "fast" (ex: don't eat between dinner & breakfast); which upregulates PPAR & downstream inhibits mTORC1 so that our mTORC1 doesn't dampen down normal nighttime autophagy & cell recuperation .

    If  a fasting thin person's tissue protein gets used to run their metabolism it first has to be de-aminated (amino acids cleaved) so that protein molecule's carbon backbone can be oxidized. If the starvation wasn't too prolonged (like we do overnight) most of that protein molecules carbon will be used to make glucose via gluco-neo-genesis &/or glycogen (via glyco-neo-genesis for back up fuel). Some who lose weight fueling via their protein do so because it takes 7 ATP to turn protein into 1 ATP of useable  energy & then will pee out lots of water to get rid of the ammonia nitrogen byproduct.


    If one still has body fat (unlike the emaciated) then the fasting level of  FGF21 (fibroblast growth factor) is what upregulates liver keto-genesis in  period of "starvation".  Since  TypeII diabetics (& many obese) have lots of  FGF21  some diabetics measure ketones in their urine to monitor if their condition is getting potentially perilous. Autophagy goes down when the amount of beta-oxidation being performed goes up;  when there is sparse gene Atg7 activity this down-regulates autophagy  and then there are less trigs building up (ie: autophagy  activity up from more Atg7 activity means more lipid droplets shunted to lyso-some for kicking out of cell to be cobbled into trigs to move around - if not excessive trigs are useful).

    Does intermittent fasting train autophagy to be better? I think in the sense that the yo-yo effect of driving the body to scavenge itself for energy substrate (ideally fatty acids & not protein) means intermittent fasting is an form of conditioning. For most the rising ketogenesis  means there was a drop in circulating insulin. It could be said that fasting/starvation forces the liver to behave insulin intolerant ( when liver autophagy is suppressed there is insulin resistance) & that when resume eating the net affect is beneficial due to hormesis. This hormesis inclines the starved faster person to re-bound with a stronger insulin signaling response. Partly that rebound is due to the exagerated degree insulin signal surges through it's intended cascades when the re-fed person's  liver & skeletal muscle cells' Akt gets phosphorylation anew (sort of a pivotal  "oh yeah/that's it/way to go/do me" phosphorylation event on the waiting serine residue of Akt).

  • Might-o'chondri-AL

    11/18/2011 9:35:59 AM |

    Hi Majkinetor,
    I see Doc's has told you above that IF & autophagy are  " likely something close to linear."  Maybe I am misinterpreting the practice of  intermittent fasting & how it plays into our liver's rhythmic genetic expression. I assume it meant close to 24 hours without food.

    +/-6 hours after finishing last meal of the day  there is a rise in lipid droplets shunted for  recycling (a kind of autophagy)  & in the liver these are designed  to be going for ketone making.  Usually our ketone body output lasts +/- 8 hours, but if one is very low carb this might differ . We also should have a  +/- 6 hours cortico-sterone peak that usually  parallels the later part of  a standard overnight ketone cycle . Circadian cortico-sterol levels being up foster the gluco-neogenesis processes we use to build a reserve for when the ketones usually decline. So to hold onto that  reserve (normally for our coming day's get up & go) those cortico-sterols inhibit glucose being taken up into non-liver tissues ( or  used up in the liver). Since insulin signal for glucose to be used is not being acted on I have likened it to being a mimicry of insulin resistance (most people will have insulin in circulation all the time)..

    What do consistently insulin resistant people like Type II diabetics manifest? Lots of muscle protein breakdown (catabolism), protein & ketones  in urine , even before breakfast  lots of trigs (from lipid droplets)  &  plenty of glucose not  being taken up into  tissues. Unfortunately this isn't the way recuperative autophagy is supposed to work, because pathological insulin resistance runs it's program even during the daytime. We are designed to recycle/restore & recuperate while we sleep at night.  Autophagy of our old mitochondria power organelles also ideally happens at night, since you don't want to lose power during an challenge.

    Anyway, so if you had your 8 hours of ketones  +  6 hours of glucose +  2 hours of glycogen filling in  that means after +/- 16 hours of not eating you are into starvation (as opposed to overnight fasting). At this stage your body nutrient sensing is registering the caloric limitation & is trying to hold off doing any cellular house cleaning because that  type of autophagy requires a lot of energy expenditure. If you have some body fat it will go into ketogenesis - but in this instance I don't consider it systemic autophagy, more like catabolism because at that stage you have to bust those fatty acids out to get at them. Calorie restriction is considered to inhibit autophagy, this does not mean no autophagy occurs just minimal autophagy .

  • Roger

    11/19/2011 11:38:14 PM |

    All above is correct, except the 600 IU recommendation, exactly because absorption varies from person to person.  
    The only way to find out if you should be taking more, less, or none st all is with regular blood tests.

  • donna

    11/20/2011 5:23:28 AM |

    Just had mine tested and it is 77.

  • majkinetor

    11/20/2011 11:12:34 AM |

    Thx M-al, for providing me new research points
    I appreciate your detailed response.

  • Dr. William Davis

    11/20/2011 4:02:06 PM |

    Unfortunately, Linda, this will be used as fuel for the "nutritional supplements are dangerous" argument.

    I think the only lesson to learn from this study is that, as we already knew, toxic levels of vitamin D are toxic.

    I advocate testing vitamin D twice per year and I aim for 60-70 ng/ml.

  • Dr. William Davis

    11/20/2011 4:04:52 PM |

    Fenofibrate works to reduce triglycerides, Kenneth, but I have seen almost nobody not respond to the mix you quoted.

    In other words, even if you start with triglycerides of 2000 mg/dl--extremely high--it virtually always drops with wheat elimination and dramatic reduction of carbohydrate and omega-3 fatty acids. While fibrates work to reduce triglycerides, they are almost never necessary.

    So I fear there is something wrong in what you are doing, e.g., insufficient diet change.

  • Dr. William Davis

    11/20/2011 4:05:28 PM |

    Yup, this is the stuff that the dietitians are reading and following.

  • kenneth

    11/20/2011 6:28:36 PM |

    I'll be the first to admit my diet change or at least consistency, is not all that it might be.  Going wheat free/very low carb is a tough deal, especially in light of what you say as far as even one cheat day a week effectively undoing your blood chemistry for a week afterward.  

    I should clarify that fish oil DID help, considerably. My TG was never insane high like 2000, but upper 400s with very low - upper 20s HDL, and God knows what sort of other particle problems, as I haven't done a VAP or NMR.  Just by taking fish oil and eliminating egregious things like lots of pizza and booze, my levels dropped by about a third. Niacin at a gram a day did nothing for TG for me, but did give me a few points on HDL. I have been unable to tolerate a higher dose despite careful titration, and for reasons beyond flushing.  When I was really on top of everything with diet and exercise, it dropped further, but never below 160 and HDL was still unimpressive. I suppose the tricor could work one of two ways, either pharmacologically or  the side effects might turn out to be so intolerable that wheat free discipline doesn't look so bad anymore!

  • fred hoy

    11/20/2011 7:59:46 PM |

    My doctor told me I was plugged, my arteries lined with plaque.
    I need to change my ways today or have a heart attack,
    eat more fish and drink more wine and do more exercise,
    for then you will extend your life, to tell more truths than lies.

    The doctor ordered me some drugs to take each day for sure.
    There is no guarantee of cure, except to make me poor.
    For everywhere both far and near, the rich and poor will die.
    Of heart attack and stroke and in their graves they’ll lie.

    Along came Linus Pauling with his saving protocol.
    He said to drink more orange juice, with a little alcohol.
    The truth that you must know to keep your arteries clear.
    Is not as simple as his words, you must not harbor fear.

    The cure to keep you healthy, is more than vitamin C,
    Amino acids, niacin, and anti-oxidant teas.
    Along with fearsome exercise and cleansing of your gut.
    Remove your mind from prejudice, think thoughts not from your butt.

    It’s been 2 years, since my doctor said my heart is full of fat.
    With Linus Pauling’s protocol, each day I firmly sat.
    My cardio said I should know my calcium score, so he scanned my heart.
    If its under 10 he won’t see me no more.

    The pain is gone, mchest is clear, my pressure’s nice and low.
    When I climb a hill I chug along, my legs just seem to flow.
    My doctor checked my score, he dropped his jaw in awe.
    A zero faced him squarely, thats exactly what he saw.
    yipee yiyay yipee yipee yiyoo learn linus paulings protocol.he song is based on my true experience. for complete story visit "healthyheartfredhoy.com"

  • LindaS

    11/20/2011 8:24:06 PM |

    Thanks for clearifying this Doctor Davis. It seems like everything the  media tells us Re: supplements,  is done in a frightening, alarmist fashion. Except when speaking of pharmaceuticals such  statins or anti-depressants, etc etc. then "all' is good and safe. You can see who holds the money bags!!!!

  • Dr. William Davis

    11/21/2011 1:34:30 PM |

    Yup. Sad, but true.

    Billions of dollars buys plenty of clout and attention. This is why conversations like this count: It is part of our effort to be better armed against it.

  • Dr. William Davis

    11/21/2011 1:35:49 PM |

    Wow, Fred, that's great!

    Now, could you do it in haiku?

  • Dr. William Davis

    11/21/2011 1:37:18 PM |

    Hi, Kenneth--

    HDL will not show its full potential until triglycerides are 60 mg/dl or less. Wheat-free, by the way, is no sacrifice in my mind; it is the most liberating health strategy I know of.

  • Ensues

    11/22/2011 9:24:55 PM |

    Hi Kenneth-

    I am just exactly like you.  Nothing I do budges my tri's or my HDL.  I did Tricor the largest dose possible and together with fish oil, low carb, vitamin d etc I got down to 220.  That's the lowest I have ever seen it.  I personally had no side effects with Tricor.  I quit after a couple of months because I loathed being on a daily medication.  Last reading was 600 and I eat very low carb.  Very frustrating.  Good luck!

  • alfredoe

    11/22/2011 11:22:03 PM |

    Omega 3 from flaxseeds is in a chemical form (ALA) that makes it ineffective for triglycerides control. You need omega 3 in the EPA and DHA chemical form (this kind of omega 3 is ALWAYS from animal origin, never from vegetable origin).

    You should get your omega 3 from fish, cod liver or krill oil. That is the way to lower your triglycerides and raise your HDL cholesterol.

    Please read http://www.omega-3-fish-oil-wonders.com/fish-oil-and-heart-disease.html

  • alfredoe

    11/22/2011 11:35:27 PM |

    I am sorry to contradict no wheat, or low carb, is a BIG sacrifice for many.  I see real carbohydrate addicts every day. I am addict to corn in all its forms, it is a big pain.

  • Kenneth

    11/23/2011 3:41:20 AM |

    Maybe what we need is a strict diet of nothing but iceberg lettuce and a brisk walking program from one end of Australia to the other! Smile I'm going to give the Tricor a shot and see how it does.  In theory it could chop my TG in half from 329 where it last was. Maybe a third is more realistic. IF I get no nasty side effects, the daily drug thing doesn't bother me. I take a handful of supplements twice a day. I suppose I'll keep cracking on the diet and exercise bit too.  I too had hope to do it all without meds but at 41, I figure I don't have a lot of "watch and wait" time left. I got buddies not very much older than me going down with strokes, another who just got home from a five-way bypass. I want no part of that scene!

  • Justin

    11/28/2011 10:25:12 PM |

    Hi Doc,

    Excellent blog. Seriously. You are changing people's lives.

    I'm a firefighter and VERY active, and it's pretty obvious a "low" carbohydrate diet isn't going to work well for me. I've tried it, and the performance hit is significant.

    How would one find a balance between enough "safe" carbohydrates to support activity levels (potatoes, limited rice if no GI issues are evident, tons of vegetables), and keeping those HDL, triglyceride, and particle size distribution numbers looking ideal?

    Thanks a ton,

    Justin Arnold

  • chessguy

    11/30/2011 11:24:34 PM |

    Hi folks,
    I am an unmedicated diabetic and my fasting blood sugar is now around USA 85, uk reading is 4.7,

    my previous hb1ac has always been 5.8 but this time I expect it will be close to 5.0 much better.

    My plan is very lowcarb , and fairly high fat,circa 20 carbs per day in total.

    I am only about 10 pounds 4 kilo overweight max.

    In the last 4 weeks I have lost 11 pounds circa 5 kilo on the very low carb high fat diet/ with ligh exercise too.

    My aim is to lower my cholesterol without statins if possible, and to loose a few kilos, And reduce my Hb1ac.

    My energy levels are fantastic , my vit D was around 40 a year ago it is 70 now as I have been on a few sunny holidays and supplements of circa 2000iu vit d daily.And fish high in omega  3 times a week.

    The question is the big rise in LDL normal, or any ideas I can reflect on.????

    Did I take the test too early ?? ##
    Has any one else experienced this.??

    Has any one taken crestor or some statin for a while til this levels out hopefully,

    Any one taking a statin while on a low carb high fat diet and why , did the low carb high fat not work ??

    MY total cholesterol and HDL have gone "beserk" , but triglycerides have lowered.

    Total Cholesterol: << this was taken two weeks ago it was only the third week into my very low carb high fat diet,#
    9.8 mmol/L = 382.2 mg/dL

    LDL Cholesterol:
    7.6 mmol/L = 296.4 mg/dL ~ My ldl has basically doubled here ###

    HDL Cholesterol:
    1.46 mmol/L = 56.94 mg/dL slight improvement here

    1.54 mmol/L = 137.06 mg/dL big improvement here THEY HAVE NEVER BEEN SO LOW

    Test taken on 29/07/2011 <<<< Before the very low carb high fat diet.

    " THE UK & USA MEASUREMENTS ARE SHOWN side by side ".

    Total Cholesterol:
    5.8 mmol/L = 226.2 mg/dL

    LDL Cholesterol:
    3.4 mmol/L = 132.6 mg/dL

    HDL Cholesterol:
    1.37 mmol/L = 53.43 mg/dL

    2.25 mmol/L = 200.25 mg/dL

  • Dr. William Davis

    12/1/2011 4:18:21 AM |

    Hi, Chess--

    Recall that LDL is a calculated value and thereby an incredibly unreliable value. The fact that triglycerides have dropped so precipitously suggests that LDL has converted to large and will overestimate true LDL.

    What you need is a genuine lipoprotein panel, e.g., NMR, once weight has plateaued for about 2 months.

  • Dr. William Davis

    12/1/2011 4:24:10 AM |

    Thanks, Justin.

    The "performance hit" is likely temporary and tends to diminish or disappear within a few days to weeks, as your body converts to a fat burning metabolism.

    The only time you need to actually supplement carbohydrates is during an exceptional long-distance or long-duration effort.

  • Kenneth

    12/2/2011 10:28:54 PM |

    What's your sense of the prospects of the CETP inhibitors now in the pipleline? It seems like they managed to engineer out the blood pressure problems caused by aldosterone or whatever it was, and they show phenomenal increases in HDL. IF any of these pan out and the HDL produces is actually functional, I'd be all over that.....

  • JLMK

    12/6/2011 4:31:53 AM |

    For more info on statins, please see Stephanie Seneff's take. She recently presented at the Weston A Price conference in Dallas.


    Best wishes,

  • Dr. William Davis

    12/6/2011 5:25:39 PM |

    Stilll much to learn about those agents.

    However, in the meantime, I am witnessing HDL values of 80 mg/dl and near-complete or complete elimination of small LDL with the diet. By the time the CETP inhibitors come out on the market, I don't think we will need them.

  • Bob

    5/2/2012 7:42:59 PM |

    Hi Dr Davis,

    I am striving to approach the 80 marker, although my HDL has not been that high. In 2008 it was 53 with a total cholesterol level of 194. Trigylcerides were 46. Glucose was 93. I am a 6 foot tall, 55 year old guy and 178 lbs.

    With the help from a Naturopath, I have added 750mg of Nicotinic Acid (Slo niacin) per day to lower a slightly elevated level of LPa of 16mg. and I have large buoyant LDL. The results of a few months on the slo Niacin is that my Total Cholesterol is 175, Trigylcerides are 22, HDL is 75, and LDL is 96. My glucose tested at 96.Liver tested normal, slightly elevated kidney function.

    My question is on the Niacin and glucose levels- I understand that Niacin will increase glucose, but how do I go about lowering it? I try to eat low gylcemic, try to eat low carb- certainly no refined carbs, (about 100 grams a day)and I excercise regularly.

    What else can I do to get my glucose down and move the HDL up? Thank you, Sir.

  • Charles

    7/7/2014 1:14:51 PM |

    500 mg of otc niacin gives me trigs of about 49, HDL of about 69 and Iranian LDL of about 62. 750 mg gave me trigs of 34, Iranian LDL of 34 and HDL of 57.