What to Eat: The diet is defined by small LDL

9. April 2010 William Davis (15)
I approach diet from the perspective of small LDL particles.

Small LDL particles have exploded in frequency and severity in Americans. It is not at all uncommon to see 70% or more small LDL particles (i.e., 70% of total LDL particle number or Apo B) on lipoprotein testing. (I saw two people today who began with over 95% small LDL.)

Small LDL particles are:
--More likely to persist in the bloodstream longer than large LDL particles.
--More likely to adhere to components of atherosclerotic plaque.
--More likely to gain entry to plaque.
--More likely to be taken up by inflammatory white blood cells which, in turn, become the mast cells that fill coronary plaque.
--More likely to be oxidized.
--More likely to be glycated (8-fold more likely than large)

To add insult to injury, foods that trigger small LDL formation--i.e., carbohydrates--also cause high postprandial blood sugars. High postprandial blood sugars, in turn, glycate small LDL. That combination of events accelerates 1) plaque growth, 2) plaque instability, and 3) aging.

So carbohydrates trigger this sequence, carbohydrates of all stripes and colors. Not just "white" carbohydrates, but ALL carbohydrates. It's all a matter of degree and quantity. So, yes, even quinoa, bulghur, and sorghum trigger this process. I've only recently appreciated just how bad oats and oatmeal are in this regard--really bad.

Foods that trigger small LDL also trigger higher blood sugars; foods that trigger higher blood sugars also trigger small LDL. Small LDL and blood sugar are two different things, but they track each other very closely.

So, in the Track Your Plaque approach to diet, we craft diet based on these simple principles:

1) Eliminate wheat, cornstarch, and sugars--These are the most flagrant triggers of small LDL, blood sugar, and, therefore, LDL glycation.
2) The inclusion of other carbohydrates, such as oatmeal, quinoa, rye, etc. depends on individual sensitivity. Individual sensitivity is best gauged by assessing one-hour postprandial glucose.

Stay tuned for more in this series. Also, Track Your Plaque Members: We will be having an in-depth webinar detailing more on thees principles in the next couple of weeks.
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Comments (15) -

  • Anonymous

    4/9/2010 8:44:03 PM |

    How ia ApoB test used to know small LDL? Particle count exams aren't available in my area but ApoB is. So I'd like to know how to read this test.

    thankyou

  • Dana Law

    4/10/2010 12:45:03 AM |

    Dr. Davis,
    Please give us an eating plan.  You rant about people making lousy decisions with food.  We need some direction.  What are you eating?  Please tell us.  I find this part the most difficult.  I know I've improved in my quality of food.  Three times a day I need to make the best choices.  It's like being married to a nymphomaniac. You have to have to satisfy the healthy needs of your body, everyday!
    I believe you know what you are talking about.  You've improved our lives but tell us, please, what you are doing personally, day by day, to make those LDL particles small.  
    Sincerely,
    Dana Law
    San Diego, Ca
    P.S. This is a rant.  We need your help.

  • Taylor

    4/10/2010 5:48:55 AM |

    Love your blog, sir. I've been reading up over the last couple weeks--one question I couldn't find answered, though, was which glucose monitor you'd personally recommend? There are a lot of them out there on the market and I'm completely at a loss for how to tell them apart!

    Thanks for all the important work you do.

    --T.

  • ET

    4/10/2010 11:04:36 AM |

    For me, reducing carbs to <90g/day did little to improve my small, dense LDL.  My LDL particle number was over 2,000 and my small, dense LDL >1,600.  Increasing my saturated fat intake and niacin dropped my small, dense LDL to <120 in less than a year.

  • JC

    4/10/2010 11:26:38 AM |

    Many of those who live in the "green zones" have a high carb diet and yet live long healthy lives.Maybe the type of carb really is important.

  • Peter

    4/10/2010 11:47:32 AM |

    Re: the cultures that eat high carb but have low rates of diabetes (Japan) do they have low post-prandial scores and low small LDL particles despite lots of rice or corn and beans?

    I'm wondering why some very high carb cultures have so little obesity, heart disease, and diabetes.

  • Lou

    4/10/2010 2:09:54 PM |

    For people who are confused of what to eat, etc - check out Whole Health Source website. Very helpful.  Check out diabetes and diet under LABELS on the right side that Stephan explains in more details why, how, what, etc works.

    If there's a diet book that you can buy from a bookstore, Paleo Diet would probably be the best but it's not perfect. It says to avoid but it's perfectly fine and even the author changed his mind and it's fine to consume them.

    Free The Animal website has helpful information on how to make dinners.

    Dana Law, there's not need to eat 3 times a day. It's not really required. You can have two very nutritional meal with high amount of fat and feel satisfied for a long time, preferably break fast and dinner with maybe handful of snack like pecan, almond, walnut. That's pretty much how I eat. We're not programmed to eat that often anyway. That's how blood sugar stays low.

    JC and Peter, you need to be more specific... are we talking about percentage of meal high in carbs or total amount of carbs? Two entirely different things. We eat way more carbs than those people, I bet. I'd have to travel to those places to see that myself because I don't believe anything media tells us.

  • Paula

    4/11/2010 12:25:10 AM |

    Dana,
    Dr. Davis's "eating plan" is available to Track Your Plaque members.  I've been a member for over a year, and I can't tell you how much I've learned.  Check out the website at trackyourplaque.com and sign up!

  • Anonymous

    4/11/2010 7:35:20 AM |

    Dana, stop your ranting.  Your air of entitlement is annoying.  The fact that Dr. Davis graciously gives of his time to post some of his insights and advice does not make him a servant at your beck and call.

  • Anonymous

    4/11/2010 1:30:51 PM |

    ET, thanks for your post.  Some folks get carried away with Paleolithic diet or nothing. For those of us who prefer to limit our meat consumption, 2-3grms/day Niacin is a must.

    Dr D is always solid about whether his information is anecdotal or based on clinical trials.  If you would like additional supporting evidence for Niacin and its effects on LDL particle size, check out lipdsonline.org and search "niacin"

    " As in previous studies, niacin therapy had no significant effect on LDL cholesterol concentrations; however, after 3 months of treatment the number of small and medium sized LDL cholesterol particles was significantly decreased in those given niacin compared with those given placebo"

    Trevor

  • Tom

    4/11/2010 2:35:58 PM |

    I agree that I find it pathetic that someone would rant on a free website and some of the very best information available anywhere.  Please stop it now.

    Other posters who are asking about meters, etc:  please review the prior blogs that are listed alphabetically on the left.  Jeez folks, make some effort will you?

    Tom C.

  • Gina

    4/12/2010 4:28:27 AM |

    Yeah! So good to hear you speak out re the quinoa, oats and other carbs. Seems I can get clients to consider letting go of wheat (surprising) but  they now think quinoa is the nectar of the gods. 15 years ago I had a hard time selling even a handful of quinoa and now it is the sweetheart of grains. go figure...oh yet  again it is about who is pushing the stuff. You suppose Ornish is involved ;)
    Great post yet again Doc!

  • Anonymous

    4/12/2010 6:45:36 PM |

    I don't see what is wrong with Dana's post..... maybe we are just a tad more relaxed, those of us who don't eat too much meat Smile
    Trevor

  • April

    4/13/2010 4:42:17 AM |

    yes,I agree that a diet high on carbohydrates and sugar makes people obese and increases the risk for them to be diabetic.

  • Anonymous

    6/26/2010 6:36:17 PM |

    Do any of the home cholesterol meters (Cholesetch , Cardiochek, etc.) measure LDL particle number (i.e. small dense vs. the large not-so-dangerous kind)?

    Would be nice to conveniently measure real ldl once a day!

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Diet: One size does NOT fit all

Diet: One size does NOT fit all

24. August 2011 William Davis (33)
Heart Scan Blog reader, Frustrated, posted this comment:

Dr. Davis,
I have spent the last 5 months eating a diet that completely eliminated all wheat products. It was very low carb, and consisted of relatively high protein (eggs, grass fed beef, grass fed raw cheese, oily fish, chicken), good level of olive oil, walnuts, fish oil (3 mg per day), raw vegetables, little bit of fruit. So I had good amount of monounsaturated fat as well as saturated fat from eggs and grass fed products.

My recent NMR showed:
LDL-p. 2,800
Small LDL particle 1700
Small HDL particle 20
HDL-C 40
LDL-C 114
Trigs. 224
Total chol 208

So I was disappointed. Where have I gone wrong? No wheat and sky-high LDL-p and 1700 small LDL particles.

This is indeed unusual. I see this perhaps 5 or 6 times over a year's time, while thousands of other people show the usual expected respone. I don't have Frustrated's lipoprotein panel prior to starting the diet, but I'll bet the starting panel was similar to this "after" panel.

The overwhelming majority of people who follow a diet like the one described--no wheat, limited carbohydrate, grass fed beef, fish, chicken, vegetables, limited fruit--obtain extravagant reductions in small LDL, increased HDL, and reduced triglycerides. So why did Frustrated end up with such disappointing results, values that potentially provide for high risk for heart disease?

There are several possibilities:

1) He/she is in the midst of substantial weight loss. When labs are drawn in the midst of weight loss, stored energy is being mobilized into the blood stream. This energy is mobilized as fatty acids and triglycerides which, upon entering the blood stream, cause increased triglycerides, reduced HDL, chaotic or unpredictable small LDL patterns, and increased blood sugar sufficient to be in the diabetic or pre-diabetic range. This all subsides and settles down to better values around 2 months after weight loss has plateaued.

2) Apo E4--If Frustrated has one or two apo E4 genes, then increased dietary fat will serve to exaggerate measures like small LDL despite the reduction in carbohydrates, LDL particle number, and triglycerides. This is a tough situation, since small LDL particles and high triglycerides signal carbohydrate sensitivity, while apo E4 makes this person, in effect, unable to deal with fats and dietary cholesterol. It gives me the creeps to talk about reducing fat intake, but this becomes necessary along with carbohydrate restriction, else statin drugs will come to the "rescue."

3) Apo E2 + Apo E4--It's possible that an apo E2 is present along with apo E4. Apo E2 makes this person extremely carbohydrate-sensitive and diabetes-prone with awful postprandial (after-meal) persistence of dietary byproducts, alongside the hyperabsorption of fats and dietary cholesterol from apo E4. This is a genuine nutritional rock and a hard place.

4) Other variants--There are probably a dozen or more other genetic variants, thankfully rare, such as apo B and apo C2 variants, that are not generally available for us to measure that could influence Frustrated's response.

5) The low-carb diet is not truly low-carb--Frustrated sounds like a pretty sharp cookie. But it's not uncommon for someone to overlook a substantial source of carbohydrate exposure that triggers these patterns. Fruit is a very common tripping point, since people generally regard unlimited fruit as a healthy thing. This does not seem to be Frustrated's problem. Others indulge in quinoa, sweet potatoes, millet or other carbohydrate sources that look and sound healthy but, in sufficient quantities, can still trigger this pattern.

6) Other--Hypothyroidism, kidney disease, nephrotic syndrome, hypercortisolism and some other relatively rare conditions are worth considering if none of the above apply.

Anyway, that's the list I use when this peculiar situation arises. If obvious weight loss is not the culprit, the next step is apo E testing. However, the wrong response is to reject the low-carbohydrate notion altogether and just limit fat, since this typically leads to uncontrolled small LDL, high triglycerides, and diabetes. It can often mean limiting carbohydrates while also limiting fats. Just as with the combination of apo E4 with Lipoprotein(a), I lump many of these patterns into the emerging world of genetic incompatibilities, genetic traits that code for incompatible metabolic phenomena.


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Comments (33) -

  • David Horry

    8/24/2011 6:03:44 AM |

    Hi Dr Davis,
    I am an apoe4 carrier. My trig=62, HDL=69; LDL-C=175 after 16 months on a carbohydrate restricted, gluten free diet. Wondering whether I need to also reduce my fat intake. But then what is left to eat? Making up the calorie difference with protein does not sound too healthy.

    David

  • Dr. William Davis

    8/24/2011 12:24:19 PM |

    Hi, David--

    I would urge you to NOT rely on the calculated LDL value, since on a low-carb diet with potential conversion of small to large LDL particles calculated LDL can substantially overestimate true LDL.

    The best: LDL particle number through NMR lipoprotein analysis. The next best: apoprotein B, widely available from nearly all labs.

    When you're armed with this information, then you can make an intelligent decision about diet changes.

  • Paul

    8/24/2011 1:43:34 PM |

    Regarding Item 6

    There was some traffic between Chris Kresser and Jimmy Moore on Twitter yesterday regarding whether low carb caused low T3 in susceptible individuals. Clearly bad news for heart health.

    I am a treated hypothyroid and this was my recent experience - I had gone low carb and ended up with an abscess in the roof of my mouth that needed antibiotics.  When tested, my T3 had fallen from 5.5 to 3.8 (RR 4 - 6.8) - however, my TSH was 0.672 (RR 0.35-4.5).  In the UK, this low T3 would normally would have been missed as there is a TSH only testing policy here unless the TSH is found to be outside the reference range - I elected to pay privately for the T3 test.

    I remain on low-carb (and wheat free of course) as it is the only approach which allows me to lose weight, and have increased my meds from 75T4+20T3 to 100T4+40T3.

    I would query whether you consider hypothyroidism to be rare. I suspect it is very common.

  • steve

    8/24/2011 6:52:16 PM |

    Hi Dr. Davis:
    What if the patient  followed the above diet, had a particle count of 2,100, but only 200 were small and HDL 69 and Trgs 66.  Would this be acceptable, and better than a particle count of 640, less than 90 small, HDL 64, Trgs 45, but on statin and Zetia?  Assume thyroid and D all normal, and Apo E3/3
    Thanks for all the input

  • Chris

    8/24/2011 7:26:24 PM |

    Hi Dr Davis,
    This post really hit home with me (and ironically this is my first visit to your site).  I had a heart attack 2 years ago (34 years old, ate well or so I thought, in great physical condition at 5'9" 150 lbs).  My cardiologist advised the usual low fat diet and pravastatin, and while my lipids are better than they were, I'm still very concerned they are not near where they should be.

    About 5 weeks ago I found the primal diet and began eating that diet.  Last week I had another lipid test and my numbers actually got worse (not by much).  Would you mind reviewing my numbers and if you have any suggestions I would appreciate it.

    8/31/2009 heart attack
    total chol 115
    LDL 74
    HDL 16
    Triglycerides 126
    VLDL 25

    07/19/2010 checkup
    total chol 138
    LDL 64
    HDL 33
    Triglycerides 203
    VLDL 41

    03/21/2011 Healthfair
    total chol 122
    LDL 69
    HDL 31
    Triglycerides 111
    VLDL 22

    8/19/2011 walk in lab:
    total chol 159
    LDL 98
    HDL 34
    Triglycerides 135
    VLDL 27

    Glucose 97
    hsCRP 1.2
    A1c 5.5

    Do you suggest giving the "primal" diet more time or do you suspect I may have another condition causing this?

  • Chris

    8/24/2011 7:36:33 PM |

    Also in May of this year I had the following tests done at the cardiologists:
    Date of service: May 13, 2011
    CAT Scan MRI & NMR
    Diagnostic Radiology X-Ray
    Cardiovascular Stress Test

    I was told everything was fine.

  • Might-o'chondri-AL

    8/25/2011 2:28:51 AM |

    Track Your Plaque once gave a desirable level of ApoB  as under 70 mg.dl as surrogate marker for the desirable LDL particle number (which is less than 700 nm/l) if one only has ApoB testing.  Maybe some one else can recall the conversion ratio of ApoB into LDL particle numbers.

    A cholesterol fractions normal transfer from HDL to ApoB is governed by  the cholesterol ester transfer protein (CETP). Genetic variants of CETP can cause differences in the numbers of  small LDL and sparse CETP can cause cholesterol to stay stuck in HDL  ( CETP has little impact on numerical % of HDL). So genetic variants of ApoB can influence the levels of cholesterol shunting around.

    In  the liver ApoB normally gets it's lipids when ApoB goes into a cell's endoplasmic reticulum. And if the ApoB doesn't improperly degrade ( ApoB needs "enough" microsomal triglyceride transfer protein SREBP-1c, the sterol regulatory element binding protein, to avoid degrading) then ApoB can pick up triglycerides to form VLDL molecules. So, if there is not enough liver SREBP-1c  then lipids can't be transferred over to make triglyceride rich VLDL; conversely lots of liver SREBP-1c provokes extra VLDL.

    Doc says carbohydrate related  post-prandial high glucose not only induces  more VLDL output  from the liver but that this is part of the mechanism whereby carbs can boost body fat. High carbohydrate intake causes extra lipo-genesis in the liver because a significant  reflex of high post -prandial liver insulin is a signal that upregulates SREBP-1c. Then SREBP-1c expression rises and that in turn activates genes for the lipogenic enzymes (ex: fatty acid synthesase & acetyl CoA carboxylase),

    Rogue readings of VLDL may be due to viral hepatitis proteins, flavivirus and pestivirus, which can decrease VLDL formation and secretion while dropping levels of ApoB. Viral proteins "smear" onto lipids and this blocks SREBP-1c action and viral proteins can also "stick" on to the HDL protein fraction ApoA1 inside of the  liver cells' Golgi Apparatus. Thus in chronic liver disease and hepatitis circulating VLDL associated triglycerides eventually decreases so there are more non-VLDL  triglycerides in play.

  • Jack Daniels

    8/25/2011 11:49:38 AM |

    Hi Dr. Davis,

    I was just wondering, due to many healthy cultures including the kitava, okinawan's...etc, who indulge in rather high carb intakes and retain rather pristine health, is it possible that high trigs, low hdl..etc may just be a lipid profile reflecting high carb* intake rather than suggesting atherogenic buildup ?

    *when based on safe starchy type carbs

  • Dr. William Davis

    8/25/2011 3:42:09 PM |

    Hi, Paul--
    In the population I see, hypothyroidism is exceptionally common, both in people on low-carb but also in people prior to initiating their low-carb efforts. So, without a formal analysis, I'm skeptical that low-carb in and of itself causes free T3 to drop.
    There are also numerous inhibitors of the 5'-deiodinase enzyme that converts T4 to T3, including perchlorate residues from fertilizers in vegetables and polyfluorooctanoic acid, the residue of non-stick cookware, just to name a couple.

  • Dr. William Davis

    8/25/2011 3:43:29 PM |

    This is the BIG unanswered question. Sadly, there are next to no data that speaks to this question.
    My day to day answer has been to 1) eliminate small LDL, then 2) maintain LDL particle number 1500 nmol/L or less. But that is pure speculation on my part.

  • Dr. William Davis

    8/25/2011 3:45:22 PM |

    Hi, Chris--
    Something doesn't compute: Every panel you list is the pattern of excessive carbohydrate consumption and/or sensitivity. So something is sneaking through. There is no question that a "primal" or low-carbohydrate approach works for this pattern.  

    You might also have an Apo E2 gene that amplifies carbohydrate sensitivity.

  • Dr. William Davis

    8/25/2011 3:47:01 PM |

    Hi, Might--
    As always, you are an incredible fountain of unique insights!

  • Dr. William Davis

    8/25/2011 3:47:44 PM |

    Sorry, Jack, I didn't understand your question. Could you rephrase?

  • Chris

    8/25/2011 4:28:55 PM |

    Thanks.  I've only been eating primal/paleo for about five weeks, so only the last panel would reflect this (if thats enough time to be reflected in my lipid panel).  I will re-test after another few months.

  • Jack Kronk

    8/25/2011 4:53:55 PM |

    Dr Davis. Jeez. This sounds similar to my story (Frustrated's #s). I have eaten Paleo for over a year now, I have done exceedingly well with body composition in that time. See my "Share You Paleo Before and After" here ---> http://paleohacks.com/questions/7058/share-your-paleo-before-and-after/28493#28493. But this only adds to the confusion for me (and others).

    For some reason, my labs came back on July 8, 2011 with small dense LDL and pathetic HDL at 40, despite a diet rich in GF beef, pastured eggs, bacon, pasture butter, coconut oil, ghee, veggies, starch and fruits only for carb sources, etc etc. I spend mega money to eat well. We don't mess around. I posted my VAP panel results on PaleoHacks last month and it has resulted in a lot of attention on this very subject. Chris Masterjohn weighed in with his thoughts. Dr Kruse wrote a blog all about it.

    http://paleohacks.com/questions/50347/hack-jack-kronks-vap-test-results

    I will be retesting again in about a month, as I have made some changes, like eliminating bananas, less heavy cream and pasture butter, etc.

    My lab said it's $390 just to do the ApoE test. Is this a normal price? If not, where do you recommend people get the testing done?

    I'm genuinely confused. It's like my body is saying... "Yes Jack. Good job. I am very happy with what you are eating. I will continue to keep fat off and pack on muscle." But then my heart is saying "Nooooo. Stop!!"

    How can this be?

  • Jack Daniels

    8/25/2011 5:29:06 PM |

    I was questioning if your pathological interpretation of a blood lipid profile that exhibits low hdl and high triglycerides, could instead just be a reflection of a high carb diet rather than suggesting an increased risk for CVD. I was referencing a couple high carb cultures, such as the Okinawa and the kitava, who exhibit a similar lipid profile but have very small incidence of CVD. Compared to other cultures with similar lipid profiles, such as the Swedes and Americans, who have much higher rates of CVD would suggest it's more about quality of blood lipids rather than their certain partitioning. Hopefully that's a better re-phrasal?

  • steve

    8/25/2011 5:57:08 PM |

    This is the BIG unanswered question. Sadly, there are next to no data that speaks to this question.
    My day to day answer has been to 1) eliminate small LDL, then 2) maintain LDL particle number 1500 nmol/L or less. But that is pure speculation on my part.

    My understanding related to your above comment is that large LDL is nearly as athrogenic as small LDL and that you want the particle number low with mix between largle and small LDL taking secondary importance.  Of course, that is based on a diet that the avg american consumes,  and not on the low carb with wheat sugar and cornstarch elimination you advocate.
    Am i under a correct understanding regarding large LDL being dangerous as well and therefore the need to minimize this even with your dietary recommendations?  Also, i thought you advocated a total LDL particle number to approach 600?  Is your 1500 number a revised viewpoint based on newer diet or clinical observations?
    Thank you again.

  • Might-o'chondri-AL

    8/25/2011 7:53:36 PM |

    Server error blocking me again ... testing after hour passed.

  • Might-o'chondri-AL

    8/25/2011 8:49:34 PM |

    ApoE is crucial to VLDL & chylomicron formation. Variant ApoE 2 less efficient at transfering lipids to liver and is binding lipids up an extra +/- 2%; result is that lipids take longer to clear from circulation and more can go wrong. From my notes, here is the rate some ancestral populations have at least 1 copy of ApoE2: 2-4% of Mexican-american & American Indian, also  3-4% of Japanese & West African. There is 0% of South American Indians with ApoE2 and one wonders which variation of  ApoE  might be in Kitava melanesians. .
    ApoE4 degrades easiest of all ApoE forms, leaving protein fragments in cell's cytosol which then can affect a mitochondria's lipid binding region impairing the performing of  tasks. In addition ApoE4 fragments diminish gene PPAR gamma expression; and this depresses the desirable bio-genesis of mitochondria. The affects on mitochondria may be why high levels of dietary fat is problematic for ApoE4 individuals; there may be too sparse output of viable mitochondria and mitochondria membranes are involved in how efficiently we burn fat or glucose.  .
    In light of these ApoE4 nuances it is interesting to know that fasting raises free fatty acid levels (from fats in the body and not loose fats from recent food); and then those free fatty acids upregulate  gene for PPAR gamma in the liver. Fasting makes one put out ketones  because of the extra PPAR gamma programing and this ketogenesis is also one way that activating more PPAR gamma improves insulin sensitivity. This suggests to me that individuals with ApoE4 may (?) find some benefit from modified fasting; possibly something like decidedly fewer meals in a day and also simply not grazing on snacks (ie: in addition to just trying to select what foods to eat) between meals that are regularly spaced apart (ie: very early breakfast to let meal times spread put more evenly) .

    Finally again from my notes, here is the rate some ancestral population have at least 1 copy of ApoE4: .14-19% Germans & Finns, also 7-12%  French & Italians. Of course America is one of the world's melting pots so an individual's propensity for ApoE 4 & ApoE 2 is hard to pin point.

  • Jack Kronk

    8/25/2011 9:02:36 PM |

    This is fascintaing Might. I have been guilty of snacking too much. All healthy snacks, but still the concept of grabbing bites of delicious foods between meals might be messing with my liver. For my VAP test, I did not fast. Chris Masterjohn believes this was the reason (or at least the reason for dismissal) of my increase in triglycerides in the blood. I am most concerned about my low HDL, because if I raise my HDL, I believe my LDL will become more dominantly pattern A.

  • Paul

    8/25/2011 11:04:33 PM |

    Thank you for the reply.  I would like to share a speculation.  Strict low carb means gluconeogenesis means an increased cortisol demand? OK in young fit Paleo men, but what about long-term un(der)treated hypothyroid individuals?

    In "Safe Uses of Cortisol", Dr William Mck Jefferies (p. 183/4) observes that low dose (20mg/day) of hydrocortisone taken by a patient with hypothyroidism increases T3,  lowers T4 and improves patient energy levels suggesting such low dose cortisol enhances T4 to T3 conversion.

    Could VLC, by putting demands on potentially weakened adrenals, have the opposite effect?

  • Might-o'chondri-AL

    8/26/2011 12:10:58 AM |

    HDL molecules hold triglycerides (there are 45 different variations of triglycerides in circulation, which are based on what their esterified fatty acid component is), cholesterol esters (about 13 - 27% of the HDL surface particles), shingomyelins and glycerophospholipids. HDL's principle proteins are +/- 70% ApoA1 and +/- 20% ApoA2;  yet any changes in the ratio of ApoA2 from genetics (Kitavans?, I propose so) or drugs (ex:fibrates) can have effects.  

    Usually people with low levels of  HDL have more trigs on their HDL surface (compared to those with high levels of HDL) and low HDL is associated with the passing of more cholesterol esters to VLDL & chylomicrons. Also, when HDL trig levels go up that makes it easier for the liver enzyme hepatic lipase to cleave off more ApoA1 for the kidneys to clear away; and that further tends to keep HDL levels low.  

    In comparison people with high levels of HDL have more cholesterol esters on their HDL; which may be due in part to cholesterol esters affinity for ApoA1 in HDL. And statisticly high levels of HDL are usually associated with bigger ("large") HDL molecule size. Both large HDL and ApoA1 are considered to be more protective factors against atherosclerosis.

    I suspect that Kitavan melanesians' low HDL fortuitously correlates with a geneticly higher than normal % of ApoA2; and ApoA2 configures more deeply nestled into the HDL complex than ApoA1. It (ApoA2) influences molecular  interactions all the way to the HDL surface and limits certain lipid dynamics.

    ApoA2 holds ApoA1 off of mature HDL molecules and this results in a shunting of ApoA1 into forming up the pre-Beta HDL; these lipid poor ApoA1 configurations are great at doing reverse cholesterol transport that brings back cholesterol  to the liver for excreting as bile acids. Those pre-Beta HDL are small, yet notably excellent at taking cholesterol away from nefarious macrophage foam cells (the large HDL  molecule also picks cholesterol nicely from foam cells).

    Experiments see that preceeding type of change with fibrate drug doses, which only minimally raise HDL & ApoA1 yet increase the ApoA2 amount in HDL by over 25%. Since fibrates are agonists activating the peroxisome proliferator activiated receptor PPAR alpha it might be instructive to see if anything in the Kitavan diet is a similar agonist, such as heirloom tuber roots derived from wild yam with high diosgenin content (diosgenin is well known to affect PPAR gamma).

  • Dr. William Davis

    8/26/2011 5:15:14 PM |

    Hi, Steve--
    There really is no final word on what the desired endpoint is when small LDl has been eliminated and you have pure large LDL. In a perfect world, I'd wish for a particle number of 600 nmol/L with pure large LDL. But I'm no longer entirely sure this is necessary. But this remains anecdotal. There are no formal data, nor do I have any formal analysis of our own data on this question.

  • Dr. William Davis

    8/26/2011 5:17:32 PM |

    Hi, Jack--
    Don't know, since I've never seen any genuine lipoprotein data on these populations. Most of the data I've seen has been total cholesterol, which is far too crude to draw any conclusions from.

    Have you seen lipoprotein data on these populations?

  • Jack Kronk

    8/26/2011 5:33:12 PM |

    Might. Do you suspect that I have low HDL and highish Trigs/VLDL in the blood for this reason? I do take in a fair amount of protein (including a whey isolate daily). Also, plenty of eggs. Does dietary protein consumption have any actual affect on HDL's principle protein and/or surface cholesterol esters?

  • The Surgical Blog

    8/27/2011 3:52:44 AM |

    Yes Jack Kronk, it seems that you have low HDL and highish Trigs, I do also think.

  • Nancy Milligan

    8/28/2011 7:51:57 PM |

    Just wanted to comment. I've been a long time low carb person, gluten-free too. I also had my thyroid ablated with RAI many years ago. I have found, as have many low carbers, that my reverse T3 is very high and Free T3 is scraping the bottom or below the range.

    Unfortunately this does seem to be a common side-effect of low carb eating. It's even documented in studies on the topic.

    We had a low carb eater recently watching his LDL climb to very high levels after he began eating low carb. He started taking cytomel and his LDL is coming down very nicely.

    Did he get a sudden onset of hypothyroidism that just coincided with low carb eating? I suppose that's possible, but I do think there's something more going on.

    I'm taking Armour thyroid myself, but I still have the tendency to turn T4 into reverse T3 and I suppose that means the Free T3 can't get to the receptors. I'm going to experiment with raising my carbs a little higher and sticking to things like yams and squash for my carbs.

  • Espen Rostrup

    8/31/2011 12:33:45 PM |

    Dear dr. Davis,
    I just attended the annual cardiology congress of the European Society of Cardiology. Amongst others, the new guidelines on dyslipidemia were presented and I had the opportunity to ask the working group the question you mention above in your first of opportunities : What about measuring lipids during an ongoing substantial weight loss? The were not able to give me a proper answer.
    Do you have any scientific references saying that weight loss induce a temporary dyslipidemia or is it based on your experience?
    I would be most thankful for your comment on this.
    Best regards
    Espen Rostrup, MD, PhD-fellow
    Bergen, Norway

  • Dr. William Davis

    9/2/2011 2:56:29 AM |

    Dr. Rostrup--

    Unfortunately, I know of no published data documenting this effect. However, I have seen it hundreds of times. It is, in fact, quite predictable: drop in HDL, rise in triglycerides, variable small LDL effects, increased blood glucose. It all subsides and improves over time.

    It would indeed be an interesting study to chronicle the changes serially in a small number of people.

  • Dana

    9/8/2011 8:28:14 PM |

    I am also seeing a heck of a lot of omega-6 intake there.  Also, the healthfulness of monounsaturated fats is a bit overstated.  I've heard of studies where they had 3 groups of people.  One got their normal saturated fat, one group replaced the saturated fat with olive oil and the third group replaced the sat-fat with corn oil.  The corn oil eaters did the worst in health outcomes, but the olive oil group wasn't great either--both groups that replaced the sat-fat did more poorly.  I've heard of other studies where lard was compared with olive oil and the lard-eaters turned out better.  Bottom line, the human body seems to like saturated fat best.  (Lard is not as saturated as butter, but it is more saturated than olive oil.)  If I were in a position to make medical recommendations (I'm not), I'd tell someone like this to ixnay on the plant oils for a while and see what happens.

    It should be noted that one of the more dubious selling points of grass-finished meat is that it is lower in saturated fat.  To me, this is not a selling point.  If this person were only getting PUFAs from their grass-finished meat it would be one thing--at least then it'd be closer to a 1:1 omega-6/omega-3 ratio.  But that's not what's going on here.  If they were just eating the fish they might still be OK (depends on the fish--cold-water is better).  But they're adding in walnut oil and chicken consumption and those are going to add more omega-6, even if the chicken's pastured.

    I'm curious what this person's inflammation markers are.  If they're off the map the LDL may still be high because the body's trying to repair the inflammation.  That would explain the low HDL too; LDL takes cholesterol out to the body from the liver, and HDL returns it to the liver.  If the cholesterol is *needed* elsewhere in the body then of course it won't be returned to the liver.

    Even if inflammation markers are normal, this person's diet may not be meeting their needs for saturated fats in the cell membranes, which may mean they need more cholesterol in their cell membranes to try to make up the deficit.  Not an ideal situation.

    Get the PUFA reduced, get the inflammation down if any, see what the lipids do and then we can talk about weird genes.  Absent the necessary DNA profile we really don't know, anyway.

  • Dana

    9/8/2011 8:31:06 PM |

    "just eating the fish" = in addition to the pastured beef.  I would not drop beef in favor of fish, there's too much good nutrition a person would be giving up, but fish in addition to beef's not bad.  Chicken used to be a luxury food, you had it on Sundays if then.  Best that it's relegated to that role again.  The white meat is too dry and the dark meat's rife with PUFAs.  Other fowl are not much better.  A foray into the USDA's nutritional database is an eye-opener.

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Are you a tree?

Are you a tree?

5. March 2009 William Davis (6)
I assume you answered no. Then why would you consider taking the plant form of vitamin D (ergocalciferol)? That's the prescription form of vitamin D, often dispensed as 50,000 unit tablets.

There's nothing wrong with plants. Some of my favorite foods are plants, full of nutritional value.

Then why shouldn't vitamin D2 from plants be every bit as good as the human form of vitamin D?

I believe the issue boils down to taking hormones from non-human sources. (Remember: Vitamin D is a hormone, a very powerful one at that.) Plants can be wonderful sources of flavonoids, fibers, protein, fats, vitamins, minerals, and other healthy components. But hormones?

There are other examples of non-human hormones being given to humans with undesirable or unpredictable effects:

--Xenoestrogens, phytoestrogens, and non-human mammalian estrogens--While non-human estrogens may partially mimic human estrogens, they can also block estrogen effects, or exert altogether novel effects. Non-human mammalian estrogens like Premarin can exert very peculiar (side-)effects, despite their role as prescription estrogen supplementation in humans.

--Progestins--The synthetic versions of human progesterone, like their non-human estrogen counterparts, exert weird effects that are a world apart from real progesterone.

--Sterols--Similar in structure to human cholesterol (while not a hormone, a building block for hormones), sterols have been used to reduce intestinal cholesterol absorption. However, if sterols are absorbed into the blood, they can enormously accelerate growth of atherosclerotic plaque.

--Anabolic steroids--These modifications of the testosterone molecule build muscle, but also cause liver cancer, kidney failure, violent behavior, suicide and homicidal behavior. That's not normal.

Outside of a pharmacologic effect (e.g., prednisone in place of human cortisol), there is no reason to take a non-human hormone in place of a human hormone. For that same reason, there is NO reason to take plant vitamin D2 (prescription or over-the-counter) in place of human vitamin D3.

If the non-human hormone is identical to the human form, then there is no difficulty. The best example of this are thyroid hormones from pigs. That's what Armour Thyroid is, a thyroid hormone replacement that works wonderfully well.

You will notice that virtually all of the examples of non-human hormones substituted for human hormones share one common motivation: profit. Synthetic or modified versions are more readily patent-protectable, unlike their natural counterparts which are not.

Vitamin D2 is an anemic facsimile of the real human hormone, vitamin D3 (cholecalciferol). Stay away from it.
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Comments (6) -

  • Anonymous

    3/5/2009 5:00:00 AM |

    Dr Davis,

    I am not a doctor by profession but an engineer. I am really frustrated in trying to get to the bottom of things in the medical field. It is quite vexing when I cant decide if something is a safe practice or not. Would you please help me (and perhaps many other) understand how I can take oil-based Vitamin D without worrying about Vitamin A levels as well? Should I worry about taking Cod Liver Oil based preparations with questionable manufacturing practices which seems to include filtering to remove the Vitamin D and then adding synthetic form at the end?

    If you could get into some details, it would be very helpful.

    Regards,

  • StephenB

    3/5/2009 3:41:00 PM |

    Anonymous, you could take fish oil instead of cod liver oil for the omega-3 and take vitamin D as D3 in softgel form.

    Vitamin A can be supplemented by providing its precursors like alpha-carotene, astaxanthin, beta-carotene, cryptoxanthin, lutein, lycopene, and zeaxanthin. Supplying precursors will let your body decide how much vitamin A to make out of it. Supplying preformed retinol bypasses the body's control systems.

    Cannell et al recommended an D:A ratio of about 6:1 in IU terms ("Cod Liver Oil, Vitamin A Toxicity, Frequent Respiratory Infections, and the Vitamin D Deficiency Epidemic", a commentary piece in Annals of Otology, Rhinology & Laryngology 117(11):864-870, on page 866, third paragraph).

    Maybe it's best to avoid retinol and make sure you get enough A precursors.

    StephenB

  • Jenny

    3/5/2009 5:29:00 PM |

    The yam based forms of Estrogen have a much better safety profile than the others on the market. In fact,the worst reaction I've ever had to a hormone was to a supposedly "bioidentical" estrogens from a compounding pharmacy.

    The problem with anabolic steroids apply to bioidentical testosterone supplements too. Too much testosterone is bad for your body.

  • Grandma S.

    3/5/2009 6:13:00 PM |

    Does this mean that Benecol is not good to use in lowering cholesterol?

  • Anonymous

    3/6/2009 3:15:00 AM |

    The bit that I find most disturbing in this post is the bit on sterols. Many authorities advise us to use phytosterols or stanols to lower cholesterol. I did find one article on PubMed a while ago (but can't refind it now) suggesting that, since the structure of phytosterols is similar to cholesterol, using them to replace cholesterol shouldn't just be assumed to be a safe thing to do. Do you have any more data or links on this issue?

  • mike V

    3/17/2009 3:58:00 PM |

    I came across this post by Dr Michael Holick whom I respect, and naturally all readers here respect your findings from the front line in Milwaukee. There appear to be some differences in interpretation.
    *********
    Vitamin D2 vs. D3
    Vitamindhealth.org
    Posted by mfholick on November 27, 2008 under Vitamin D |  
    **********
    Vitamin D2 and Vitamin D3 Are They Equally Potent?

    During the past several years, there have been two studies Trang et al, (Am J Clin Nutr 68:854-858, 1998); and Armas et al, (J Clin Endocrinol Metab 89:5387-91; 2004) that have raised questions about whether vitamin D2, which is found in some supplements, used in some fortified foods and is the pharmaceutical form of vitamin D that doctors prescribe for their patients, is as effective as vitamin D3 in maintaining a person’s vitamin D status, i.e., blood level of 25-hydroxyvitamin D.  Trang et al 1998 gave healthy adults 4,000 IU of vitamin D2 or 4,000 IU of vitamin D3 in alcohol for two weeks.   A comparison of the blood levels of 25-hydroxyvitamin D after two weeks revealed that there was approximately a 50% difference in the group receiving vitamin D3 (being approximately 50% higher) than the vitamin D2 group.  This implied that vitamin D3 was more effective than vitamin D2 in maintaining circulating blood levels of 25-hydroxyvitamin D.  Armas et al 2004 gave a single 50,000 IU dose of either vitamin D2 or 50,000 IU dose of vitamin D3 to healthy volunteers during the summer and observed that the group who received vitamin D2 had a more rapid drop in their circulating blood levels of 25-hydroxyvitamin D.  They also observed that the group that received vitamin D2 had a more rapid drop in their blood levels of 25-hydroxyvitamin D3 compared to the placebo group suggesting that vitamin D2 was not only less effective than vitamin D3 in maintaining circulating levels of 25-hydroxyvitamin D, but also that vitamin D2 increased the destruction of vitamin D3.

    Based on these observations, physicians, health care professionals and patients have made an effort to find vitamin D supplements that contain vitamin D3.  However, in the United States, only vitamin D2 is available as a pharmaceutical preparation, and, thus, patients who are vitamin D deficient and treated by their physicians receive vitamin D2.  I treat vitamin D deficiency with 50,000 IU of vitamin D2 once a week for eight weeks.  To prevent vitamin D deficiency from recurring, I then put the patient on 50,000 IU of vitamin D2 every two weeks forever.  From my experience of over 100 patients on this regime for up to six years, their blood levels are sustained above 30 ng/ml which is considered to be the vitamin D sufficient range.  On average, the blood level was between 40-50 ng/ml.  Furthermore, an evaluation of their blood calcium, a measure of whether ingesting vitamin D2 at these levels, had caused any toxicity did not change.  Therefore, this regime was effective in maintaining my patients’ vitamin D status without causing any untoward toxicity.

    To determine whether vitamin D2 was as effective as vitamin D3 in maintaining circulating blood levels of 25-hydroxyvitamin D, a study was conducted whereby healthy adults received either 1,000 IU of vitamin D2 or 1,000 IU of vitamin D3 in a capsule once a day in the winter for 11 weeks.  In addition, one group received a placebo capsule and one group received a capsule that contained 500 IU of vitamin D2 and 500 IU of vitamin D3 daily for 11 weeks.  Blood levels of both 25-hydroxyvitamin D2 and 25-hydroxyvitamin D3 were determined by state of the art method using liquid chromatography tandem mass spectroscopy.  Holick et al, (Vitamin D2 is as effective as vitamin D3 in maintaining circulating concentrations of 25-hydroxyvitamin D, J Clin Endocrinol Metab  93:677-681, 2008;) reported that the blood levels of 25-hydroxvitamin D rose to the same degree in the healthy adults who took either 1,000 IU of vitamin D2 a day or 1,000 IU of vitamin D3 a day for 11 weeks.  The group that received vitamin D2 also had their blood level of 25-hydroxyvitamin D3 measured.  There was no significant drop in the blood level of 25-hydroxyvitamin D3.  To determine whether the mixture of vitamin D2 with vitamin D3 would alter the blood levels of 25-hydroxyvitamin D, the adults who received 500 units of vitamin D2 with 500 units of vitamin D3 also raised their total blood levels of 25-hydroxyvitamin D3 in an almost an identical manner as the adults who received 1,000 IU of vitamin D2 or 1,000 IU of vitamin D3 a day for 11 weeks.  The authors concluded that ingesting 1,000 IU of vitamin D2 or 1,000 IU of vitamin D3 a day during the winter (at a time when sun exposure had no influence on blood levels of 25-hydroxyvitamin D) that both vitamin D2 and vitamin D3 were equally effective in maintaining the blood levels of 25-hydroxyvitamin D.  Furthermore, vitamin D2 did not have a negative influence on serum levels of 25-hydroxyvitamin D3.  Adults who took 500 units of vitamin D2 with 500 units of vitamin D3 had similar increases in their blood levels of 25-hydroxyvitamin D suggesting that vitamin D2 taken with vitamin D3 does not have any negative influence on the metabolism of vitamin D3.  

    The authors reviewed in their Conclusion several studies that had previously reported that vitamin D2 was as biologically effective as vitamin D3 in both pregnant women and in healthy adults.  This study confirms these observations and adds to the body of scientific literature demonstrating that at least when healthy adults take 1,000 IU of vitamin D2, they can be assured that it is as effective as taking 1,000 IU of vitamin D3
    ************

    Although this a little academic, since I have been perfectly happy with D3 for years, a resolution would be iteresting.
    Any chance of an update, or a Holick interview here?
    MikeV

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