Doc
I am really confused on your recommendation on trying to get k2 from food or cheese. Since you mention there is no way to tell how much k2 you are getting. I do notice that you dont mention supplements as an option to this problem. Since you are not opposed to supplements and k2 supplements are available now, I would think you would at least mention this as the solution in the meantime.

That's because this conversation was meant to supplement a full discussion on vitamin K2 posted on the website this Blog accompanies. In a full Special Report on www.trackyourplaque.com, we have a full conversation about nutritional supplements.

There are two kinds of K2 - MK-4 and MK-7.  Natto is MK-7 and all animal sources are MK-4.  Further, Dr. Weston Price did not find any examples of healthy primitive cultures that relied on MK-7. Every one used MK-4 animal sources.

The most concentrated sources of MK-4 are butter oil, fish liver oil and organ meats (such as foi gras). Cheese is a pretty dilute source by comparison.

For years, we've advised people to avoid or minimize cheese because of saturated fat or cholesterol content. I think that there's reason to re-think this advice based on the emerging data.

Did you do any research on cheese at all before you posted this blog? Look for cheeses that have holes in it because it is a product of fermentation... All REAL cheese is fermented. It does not need to have holes to be fermented. The holes are from fermentation or culturing by a specific type of bacteria- propionic bacteria. Also, processed cheese starts off as real cheese and is then processed with heat, mechanical means, chemicals, etc. While you should definitely stay away from it because of these chemicals and the creation of oxidized cholesterol, the assertion that it is not fermented is false.

This is exactly what Ron Rosedale said back in 2004.

If the only problem is that they raise blood sugar then are they okay if you eat them with fiber/fat?  If not, please explain why..

I found that all grains, even when eaten with fat, raise my blood sugar to unacceptable levels. Grains can easily get me to over 200. Get a glucometer and see what these grains do to your blood sugar. I also found that when I want to see what a food does to my blood glucose I have to test every 15-20 min after I eat. If I test only at 2 hours I might miss the spike and be falsely reassured that I can eat that food. My fasting is in the 80's and I try to keep postprandial spikes under 110 and even that may be too high.

If you are gluten sensitive, it is very common to have problems with oats(even the ones that are certified gluten free). Corn also seems to be a a problem for a good number of people who can't eat gluten.

Sorry for disgressing a bit. Here is an excellent discussion about NIACIN and its effectiveness for decreasing cardiac events:
http://www.theheart.org/article/1231453.do
Do we have to give up NIACIN?
Renfrew

Hi Renfrew,
Statin used with niacin, anti-fungals, genfibrozil, cyslosporin and erythromycin are already known by Mayo Clinic to have the potential to trigger muscle breakdown, called rhabdo-myolysis. This sends a byproduct called myo-globin into the blood that when reaches kidneys and degrades causes kidney renal tubule obstructive damage.

HDL traffics mainly with the Apoliprotein A-1 (ApoA1), which is key to bring cholesterol to HDL for binding cholesterol molecules to transport for recycling. Compromised kidneys create a uremic environment which depresses ApoA1 bio-syntheis,  while proteinuria physically overloads the kidney tubule cells; in other words HDL ends up just carrying more triglycerides around and  HDL is not properly performing desired reverse cholesterol transport (recycling).

Statins , to be fair, are showing  good results in preventing post surgery human acute kidney failure and some other kidney cases.  Of course  niacin  in rats with chronic renal failure ameliorated hypertension, proteinuria, inflammation and oxidative stress (see 2009: Am. J. Physiol. Renal Physiol. 297, F106-F113 and follow similarly related 2010: "Niacin Improves Renal Lipid Metabolism and Slows Progression in Chronic Kidney Disease" in Biochim. Biophys. Acta 1800, 6-15) .  So my non-clinician take is that niacin use, such as Doc's, without co-administered statins is largely preventative of lipo-toxicity; whereas the experiment you read of  dosing statins plus niacin risked a potential drug interaction Mayo Clinic already warned about .

Allow me to rephrase your question: If the only problem with eating glucose is that it raises your blood sugar then is it ok to eat glucose with fats & just eat donuts?

Brilliant.

I've never heard of table sugar being rated on the glycemic index as low as 59.  Nutritiondata says 68 and I have read 70 in books.  http://nutritiondata.self.com/topics/glycemic-index#values

Thanks for putting words in my mouth wise guy.  What I was saying is that if I eat a sweet potato with enough coconut oil that it doesnt spike my blood sugar, what is the problem.  Dr. Davis said in the article that it wouldnt " cause appetite stimulation, behavioral outbursts in children with ADHD, addictive consumption of foods, dementia, etc."  If the only problem is that it spikes blood sugar and you avoid that problem, then whats wrong with a sweet potato.  But you already knew what my question was.. you just wanted to take out your frustration on me...

Dr Davis:
What is a safe level for post prandial glucose measurement?  Is it under 120, under 100 or what?  Also, are you advocating a zero carb-starch diet?

Thanks,

Thanks for giving me another opportunity to make fun of your insistence on eating anything made of glucose.  What you were saying is that if you eat a GLUCOSE potato with enough coconut oil that it BECOMES A DONUT, it WILL still spike your blood sugar, that is the problem. (ANY glucose + ANY fat = DONUTS!)  Dr. Davis said in the article "IF they don't cause (conditions & behaviors caused by high blood sugar)" and then said "That’s...very misleading." If you think the only problem (and it's NOT) is that it spikes blood sugar, and you THINK you can, but actually CAN NOT avoid that OR the other problems, then that's whats wrong with a glucose potato. But you already knew what the answer is.. you just wanted to justify & take out your glucose addiction on me…

Oops, that should read (conditions & behaviors caused by wheat). Got lost in the cuts & pastes.

Okay, so rather than speaking in generalities, answer this.  I just had a baked potato with cinnamon and melted coconut oil.  Measured my blood glucose every 30 mins for 2 hours and it didn't go over 100.  It could be and probably is because I am a triathlete and I worked out in the morning so my muscle glycogen stores were empty.  So, glucose would preferentially go to muscle.  But what is wrong with eating a baked potato after a workout.  In other words, what are these "other problems" that you mention. (I didn't eat the skin by the way, b/c of the glycoalkaloids).  

I am not trying to get into an argument with you, I really dont care.  I am just trying to get more informed.  I understand however, that Dr. Davis's information applies more to diabetics and insulin resistant, so maybe for someone active like me, its not as big a deal.  But if a potato doesn't spike my blood sugar, why, specifically, should I avoid it? Thanks

I've monitored this blog for quite a while now and either I"ve forgotten the reasons or I've never seen them, but could somebody point me to the article(s) that outline the effects of high post prandial glucose?

Thanks,

Tim

The answer is in the second half of this article posted on August 5, 2011 here: http://www.trackyourplaque.com/blog/2011/08/carb-counting.html

Hello,

I would like to add to the discussion one significant issue with quinoa; saponins. They are molecules that are supposedly a major gut-irritant, and when compared to e.g. plant and animal foods have a high likelihood to cause leaky gut and inflammation of the small intestine. And inflammation is rather counterproductive for anyone trying to lose weight.

//sami

It's just part of big pharma's racket.  The public has been propgandized to fear cholesterol, statin prescriptions are based on an antiquated calculation, and the people who set cholesterol targets have financial ties to the drug companies.  This has created a big cash cow for big pharma.

The only people to benefit from statins are middle aged men who have had a heart attack and even then, the benefit is small.  If statins were restricted to those who would truely benefit, it would mean a lot less $$$$ for big pharma.

Today's news said millions more Americans over 60 could benefit from statins to combat the c-reative protein problem. How many more so called great things will statins do for us? Is this another terrific marketing ploy?

Dear Doc,
all this NMR is black magic to me so far, besides I will wait for some advanced lipid measurements until I am at least 40.
But I suspect that the LDL size can be guesstimated from e.g. triglicerides / HDL ratio - could you please supplement your post with the figures for both persons. I suspect there will be a difference there. TIA

And if a million or so "Lauries" are given Lipitor for their 85 mg/dl  real LDL, I don't expect their all-cause mortality will IMPROVE .

Doc:

My speculation is that this is merely an effect of the huge to-market costs pharmaceutical companies must endure, owing to FDA regulations.

If people didn't have false-security -- as you have shown -- of FDA hurdles and implicit [expensively purchased] assurances, they might just take a bit more proactive, intelligent and informed approach to their own health, and maybe drug companies might go back to serving an informed consumer who no longer simply bows to an authority (the FDA) because they have the power to be who they are.

My neighbor is being lipitor by his internist because both his parents have alzheimers. At least that is what my neighbor told me.  I told him I'd never heard of that and he said he'd trust the doctor to know.

Statins don't lessen the risk of heart disease by lowering cholesterol. They work by lowering inflammation which is not what  they were designed to do and was not expected. Happens a lot - drugs being created for one thing and being found to work for something else so are then subscribed for other conditions.

Statins are powerful and dangerous drugs that block the production of cholesterol. Our bodies NEED cholesterol. By blocking its production, it also blocks Co Q10 and dolichols, and more. Side effects range from minor muscle pains to the complete destruction of muscles, kidney failure then death. Also transient global amnesia (TGA) which doesn't show up immediately and is dismissed when it does. They cause depression and violent behaviour. That's why people on statins have a higher morbidity from all other causes and not heart attacks.

As renegadediabetic  above says, they show slight benefit for middle-aged men who have already had a heart attack. Oh yeah, tell us again why we need them?

"morbidity"? Um, mortality.

Darn. Message went to wrong place. Mortality is what I meant.

[...] standard practice is to usually look at your LDL cholesterol, the value that is calculated, not measured, then–almost without fail–prescribe a statin drug. While there are indeed [...]

Dr. Davis, You're a badass, one wonderful f**king badass!

_I asked Martin what he had for breakfast: a whole wheat bagel with no-added-sugar jam. Lunch: a turkey sub on whole grain bread, no mayonnaise. Snacks: baked chips, pretzels ("a low-fat snack!")._

What do you think of Joel Fuhrman's approach? He would not allow people to eat bagels, jam, bread, chips, and pretzels. The base of his diet is veggies (half raw, half-cooked), then fruits, beans, potatoes, raw nuts, and raw seeds. Grains are at the top of Fuhrman's food pyramid.

http://www.nutritionforwellness.org/img/food_pyramid.gif

Also, when he says "whole grains", he means unbroken grains like brown rice, oatmeal, etc. Not flours, or pastas, or breads made with flour. The only breads he would allow are things like sprouted grain breads, made without any flour.

Most people who eat a low-fat diet eat bad foods. They don't eat high quality foods. Dr. Fuhrman claims to lower triglycerides and improve all other health markers, because he stricly limits foods like flour, fruit juice, vegetable oils, sugar, etc. Maybe a low-fat diet based on grains (esp flours) will raise the triglycerides, but a low-fat diet based on vegetables, fruits, beans, nuts, and seeds (Fuhrman's) wont.

Fuhrman emphasizes nutrient-density far more than people like Dr. Dean Ornish. Whole grain flours are very perishable and quickly turn rancid. Weston Price pointed this out, but most people didn't bother to listen and still don't. Here's an article about how whole grain flours cause sterility if they are stored for as little as 15 days, while flour and bread that is fresh-ground doesn't. How many are eating fresh flour? I would say <1%, maybe zero.

http://eap.mcgill.ca/Publications/EAP35.htm

Just a small correction - Dr Fuhrman's diet is not really low fat like Ornish/McDougall, the only similarity to those diets is the predominance of plant based foods.

It eliminates/restricts saturated fat and plant oils but he is VERY pro 'good' fat in it's natural packaging i.e. nuts, seeds, avocado and fish oil in some cases (he prefers DHA from algae due to mercury in fish for most people and esp pregnant/lactating/babies but for high doses still recommends high quality fish oil especially for autoimmune patients). Re the nuts/seeds/avocado - in his weight loss strategy he does limit them but a minimum level is compulsory on a daily basis and he actively encourages people to have them while maintaining ideal weight i.e. can go very high if very skinny, lower if overweight but cannot eliminate them.

Yes, a reduction in unhealthy fats (saturated, trans, polyunsaturated) helps. But a reduction in fats of all sorts is not necessary and can, in fact, worsen the problem. We learned this lesson years ago with the Ornish diet and similar ultra low-fat approaches. When you reduce fat intake significantly to <10% of calories, triglycerides go way up. In those days, it wasn't uncommon to see triglycerides skyrocket past 200 or 300 mg/dl on these diets.

Do saturated fats elevate triglyceride levels in the body?  Jim

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

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.

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.

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

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?

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.

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.

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

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.

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.

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.

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

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

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.

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?

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?

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.

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

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.

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.

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?

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).

Thanks for the excellent post! Bookmarked! Will come back again…

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.

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?

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?

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

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.

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. 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.

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.

"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.

[...] Genetics: Dr. Davis has argued that some combinations of ApoE alleles may make a  person “unable to deal with fats and dietary cholesterol.” [...]