Thank you for the link. I was just talking with hubby last night about finding a recipe for cheesecake that had no wheat/gluten and would be good for us for special treats/occasions (like an upcoming family birthday). Yay.

I never use Truvia. The best stavia hands down is SweetLeaf, either the liquid or the powder. BUT Stevia acts like insulin, in fact, Asia has been using it as an insulin substitute and comes with a warning to diabetics about using it with one’s daily  insulin shots.   I stopped using it as I don’t need to rev up by insulin production.  I’m diabetic. I still go with local honey and get the benefits of having local pollen in my body.

Both DH and I noticed the aftertaste. I figured out how to use half stevia/half sugar for a few days, then 1/4 each, then all stevia, which solved the aftertaste problem for me. I then tried one teaspoon of sugar to a quart of stevia-sweetened tea with DH - he didn't notice any weird taste. So hopefully just adding a tiny bit of sugar for 1-2 weeks will get your taste buds used to stevia.

Why do people feel the need to eat desserts?  Doesn't adherence to a consistent low carb diet eventually curb most of the craving for sweets?  One teaspoon of fruit jam should be able to quell any overweening desire.  Or is the socio-cultural programming for eating confections so deeply ingrained that people just can't live without?

I agree.  In our house (LC for years), the same logic applies to low carb "treats" that applies to low carb Frankenfoods.  Don't eat foods that are trying to be foods that you know you can no longer have.  

There is a real danger in continuing to eat really sweet foods, even artificially sweetened.  "Low carb" needs to be "low sweet".  If you hang in there, you do eventually lose your taste for it.  

As for Splenda, you can find the liquid if  you try.  And the mini tablets are minimally carby.

Both cancer & systemic fungi make energy by means of glycolysis and create demands for large amounts of sugars.  People with continuing carb cravings that won't resolve may have one or the other condition.  Otherwise I'm with you, people hanging onto sweets are still living to eat rather than eating to live.

Hi Dr. Davis,
Server blocked me elsewhere, so writing this here.
Amazake data when made from white rice (brown, short & long may each differ) =
30 - 70 % complex carbohydrate saccharides
20 - 45 % maltose (not amylose)
3 - 5 % glucose
5 - 9 % protein
3 - 5% fat
1 - 7 % fiber
0.3 - 0.4 % mineral ash
iron, niacin & thiamine

Sample 1 liter (1 quart) sauce pan Amazake home kitchen batch:
200 ml ( 7 ounce volume, +/- 200 grams) short grain brown rice rinsed and drained
bring to boil  in 2.5 times the volume water
reduce heat to low and, covered,  cook 50 - 60 minutes (until not wet)
transfer cooked rice to an incubation vessel & let cool
when cooled to  60* Celcius (140 * F) mix with 400 ml (14 ounce volume) of Koji innoculant
cover with aluminum foil (or somehow) and put where can keep warm
incubation ideal temperature is 57 - 60 * C  (with leeway)
ferment for  desired time , 12 hours sweeter and I use 22 hours
when time up pan boil the Amazake (stir) 3- 5 minutes to inactivate Koji fungi
refrigerated covered keeps weeks

Dosages mentioned previously (for 165 pound adult, and Amazake was eaten with protein and fat):
(a) " low" dose with 2 hour blood glucose ending up being same as pre-prandial blood glucose was 1/8th (by volume) of the above Amazake (rough calculation would thus be ingesting 1/8th  of  +/- 600 grams  total of original dry rice and Koji rice)
(b) "high" dose with 2 hour blood glucose rebound (suggested for athletes carbs) was 1/4 (by volume) of the above Amazake recipe (rough calculation  would in this case be ingesting 1/4 of +/- 600 grams total of original dry rice and Koji rice)

Koji innoculant ( steamed white glutinous rice infused with Aspergillus oryzae and then dessicated) used was wholesale direct from L.A. producer Miyako Oriental Foods 626-962-9633; call for your local retailer of their Koji under the "Cold Mountain" brand. They recommend double their Koji for any volume of rice substrate. Other makers of Koji proportions may be less if the Koji is less dehydrated; family business G.E.M. Cultures in Wash. mail orders their Koji and it may (?) be suitable for using less (GEM also sells spores with instructions to make your own Koji).

Dr. Davis,
Orientation for those athletes interested in experimenting with Amazake:
Innoculant of rice is Aspergillus oryzae fungal infused rice grains, called Koji; Koji has alpha-amylase, glyco-amylase, acid protease, lipase, amylo-glucosidase , acid carboxy-peptidase , chitosinase and citric acid.
Incubation lets fungal penetrate new rice substrate and fungal hyphal tip performs hydrolytic enzyme secretion.

Cooking the rice first gelatinizes the starch held in granules inside of organelles with lipoprotein membranes (amyloplasts) into 16 - 30% amylose and 65 - 85 % amylopectin which are ammenable to hyphal hydrolytic action. Koji's amylo-glucosidase enzyme digests the gel &  Koji's alpha amylase enzyme reduces molecular size of amylose, which makes it less viscous and more fluidly mobile. It is glyco-amylase enzyme that turns amylose and some of the amylo-pectin chains  into glucose.
Incubation lets the fungi grow and their mycellial cell wall builds up with the amino mono-saccharide glucosamine (a.k.a. chitosan); fungi generally have 67 - 126 mg mycelial glucosamine per 1 gram dry weight mycellium. Amazake is well tolerated by most since glucosamine is useful in colitis. Glucosamine (chitosan) is a poly-cationic bio-polymer formed when chitosanase I enzyme de-acetylates chitin (in fiber); with optimal enzymatic pH being 5.5 - 6.5. Chitosan is more acid pH soluble than chitin and under chitosanase II enzyme (working from pH 3.8 -8.5) some chitin is de-acetylated to form more oligo-saccharides.

Amazake may have biologically active high molecular weight immunological poly-anionic polysaccharide
derivatives like the poly-acetyl carboxylic acid  COAM (chlorite oxidase oxy-amylose). COAM comes about when a saccharide chain is oxidatively cleaved between 2 carbon atoms resulting in oxy-amylose, a polymer of 2 aldehyde functions;  when these aldehydes gets further oxidized they produce functional carboxyls.  Rice has aldehydes like the volatile aldehyde hexanal we smell as stored rice &/or from rice bran.

Rice, like most bean & grain carbohydrate polysaccharides, include the following in both the soluble and insoluble form: arabinoxylan, beta-glucan, cellulose, mannose, galactose, xylose and uronic acid. For us these non-starch  polysaccharides are not digestible;  as neither is fiber (made up of cellulose, hemicellulose, pectin and lignan ) since 90% of our dietary fiber is linked together by beta-glycosides that our digestive enzymes can't cleave. Arabinoxylan, mannan, galacto-mannan and xylan are considered anti-nutritional since can lower intestinal uptake of nutrients; while mannose reacts with amino groups in dietary protein to reduce the amount of certain aminos properly digested.

Koji's fungal hyphal hydrolytic enzymes include mannosidase enzymes; beta mannanase catalyses the mannosidic links in insoluble mannan polysacharides where there are galactosyl residual features.  The  so-called endo-mannanase (a manno -hydrolase) cleaves mannan and galactomannan to free up molecules like manno-triose, manno-biose and manno-tetraose that human gut Bifidobacteria can then feed on. This may be part of why a substantial dose of Amazake seems to yield more delivery of  sustained energy beyond what one would get from the usual amount of short chain fatty acids put out by gut bacteria.

Amazake incubation is a solid state fermentation, since want the minimal free fluid when culturing;  too much water and the substrate porosity is diminished and resultant depressed oxygen transport in substrate  causes fungal cell numbers to decline. A  submerged fungal ferment, when cooked rice with koji substrate is set out  too soupy can result in 3.5 times less enzymatic activity. Using  too much rice substrate mixed with too sparse koji innoculant and the fermentation won't proceed promptly due to low oxygen. Also do not stir the blend while incubating to avoid damaging mature fungal hyphae or breaking new growth.

Mannanase enzyme development in 1st day is less than 50 units/gram and this goes to a maximum of 100 units/gram after 2 days; a peak mannanase content seems to be +/- 250 units/gram on days 3-5. I incubate short grain brown rice Amazake for 22 hours; while most commercial Amazake products and home producers probably do not incubate more than 12 hours. The longer incubation is allowed to go on for the more llikely bitter flavors develop from oxidation of the bran's oil content;  yet the bran is desired for it affords better beta- mannanase and beta-mannosidase enzymatic formation.

Amazake has exceptional anti-oxidant properties; with longer incubation time this activity increases. Amazake also raises the bodies ability to inhibit lipid peroxidation; so concern over any of rice bran's oil oxidation is probably moot.
END

You don't mention liquid surcralose (Splenda)  -- which has all the 'benefits' of sucralose without the maltodextrin.  I use it and nothing else.

Wow, Might. You are a walking Wikipedia!

Thanks for the incredible insights.

I have never been able to find liquid Splenda in stores in the U.S.  If it's there, what brand name is it sold under?

I use Sweet Leaf as well. It is in the powder from. the box states no chemicals,no alcohols, no erythritol, no ethanol or menthol,, no aspartame, no sucralose, no maltodextrin, no dextrose or additivees. Seems clean to me. Any thoughts as to problems with this product.

Doc, also notice the removal of all of Might's comments from Guyenet's site. This speaks for itself, as to where the truth lies. Might is truly a wonder and knows what he's talking about.

What does that mean, that the comments from Guyenet's site are removed? Stephan removed them, or Might removed them? I've traded comments with Might over there dozens of times.

I just use pure Stevia powder, which is gauranteed to be at least 95% pure stevia crystals (like the liquid stevia, on in teh form of powder. The brand I use is Stevita. A tiny little 0.7 ounce conainer lasts FOREVER! You only need a tiny pinhc of it for coffee. It doesn't exchange well versus sugar as a substitute, but adding a little to whatever you might be baking or making can help with using less of whatever other sweetener you may need to use.

Dear Dr. Davis,
It’s a great pleasure to read your blog. I find your post very informative. Thank you for sharing.
As a reader, I consider your writing to be a great example of a quality and globally competitive output.
As a moderator for Physician Nexus (a community for physicians) I would like to share your genuine ideas and knowledge. With this you can gain 1000 physician readers on Nexus.
We would love for you to visit our community. It's free, takes seconds, and is designed for physicians only - completely free of industry bias and commercial interests.
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On behalf of the Physician Nexus Team
www.PhysicianNexus.com

Stephan who hosts the WholeHealth blog is smarter than me &  the removal of my comments there came from someone using my computer. These days I do not have the time to follow Stephan's blog, which has nothing to do with validity of his approach.

Marlene,
I buy it at SuperSupplements or at Whole Foods. Any nutritional supplements &vitamins stores should carry it. If you live in a place whch doesn't havenay -> use Amazon. It's simple .

Whoops - I thought you meant Stevia. Liquid Splenda is at amazon as well

Dr. Davis--

I'd like to recommend ZSweet.  It's a stevia/erythritol blend but isn't a Big Ag product like Cargill/Coca-Cola's Truvia or Pepsico/Monsanto-er-Merisant's PureVia.

It's funny how Stevia was banned by the FDA in the 80s, only to be given the GRAS label in 2008, which just happened to be the same year that Truvia was launched.  Coincidence?

Hi, Serge-

I have no doubt that the clout of Cargill pushed Truvia through. I wasn't aware of ZSweet--thanks!

I am absolutely thrilled to have found this blog.  I've been extremely cautious of sugar and sweets since my mother was diagnosed with diabetes when I was a child.  Unfortunately I did fall into the "healthy whole grains" trap for a while, but have kept my daily carbs between 50-100 for many years now.  I like Stevia products, but unfortunately they leave me with a slight headache.  I've been (sparingly) using Volcanic Agave Nectar for years, mostly in tea and for the occasional baked good.  I understand that due to the rich soil in which it's grown, and minimal processing, volcanic blue agave has a lower glycemic index-load than other traditional agave nectars, at 27.  

Am I doing myself harm by using it?  I'd like to try the liquid Splenda, that contains no maltodextrin.  Thank you Elenor and Stefan for mentioning it, but should I be concerned about its processing?

I'm not big on Truvia.  

From what I've heard from other diabetics erthyritol doesn't have the GI side effects of most sugar alcohols and has a lesser effect on bg, but even so... I prefer a plain stevia powder.

I don't think erthyritol has been around long enough to know what it's side effects may be, that it doesn't raise bg much and doesn't cause GI distress isn't good enough. There's any number of other bad side effects that exist in the world besides those two.

Stevia is food.  Granted, the plain white stuff is relatively refined, but I still feel better about it than erthryitol.  

Susan, agave nectar has almost no GI effect because it is fructose, not glucose.  It has MUCH more fructose than HFCS.  Search this blog for a long list of the bad stuff that fructose causes.  I'm a diabetic, and I'd seriously rather eat sugar than agave.

The letter points out how critical adequate Vitamin D intake is when pregnant or lactating.

To add to that point:   an unfortunately large number of women experience pre-eclampsia during pregnancy, which often is fatal without aggressive and rapid medical intervention.   In Sept 2007, a study reported that women will low level of Vitamin D increased their likelihood of pre-eclampsia by FIVE-FOLD.

Also, perinatal cardio myopathy occurs with 1 in 3000 women in the USA, and the rate is hire for black women.  It would not be surprising if it turns out this is linked to Vitamin D also.

With the massive amount of info and research supporting the importance of vitamin D, it seems that the failure to prescribe adequate amounts of vitamin D intake is nearly criminal.

I was wondering if there is benefit to taking Vitamin D if ones level is in the normal range?

This is curious, given that in his book 'The South beach heart program', Agatston talks quite a bit about "advanced blood tests", including LP(a),and lipoprotein subfractions. I wonder if hethinks otherwise now

I ran into someone that met this doctor and she asked him what diet he eats, thinking he would be following his own.  Apparently he follows a more Paleo type of diet rather than those "healthy" whole grains he espouses in his books.

Isn't that interesting!

If I had to choose from a menu of popular diets that most closely approximates what we do in the Track Your Plaque program, it would be quite close to the Paleo Diet as articulated by Loren Cordain.

I'm surprised by that.  The Paleo diet is an extraordinarily high meat-oriented diet (the author suggest that about 55% of calories will come from meat.)  Since dairy and soy are forbidden, almost all protein must come from meat, fish, or eggs.  The diet is similar to Atkins, except that the Paleo diet makes a nod to healthier fats like flax oil, which he suggests rubbing on lean meat before serving.

On page 26 of his book, Cordain describes a 25 year old female who follows the Paleo diet.  He indicates that on a typical day she will get about 190 grams of protein.

According to NutritionData.com, each of the following contain 190 grams of protein:

31 large hard-boiled eggs

1 lb. 11 oz of salmon

1 lb. 8 oz of turkey

1 lb. 8 oz of Sirloin

1 lb. 8 oz pork chops

Six 1/4 lb. hamburgers

Basically, a pound and a half of meat.  Using the traditional "pack of cards" portion size (three ounces), a follower of the Paleo diet would be consuming eight portions of meat per day.

I'm no vegetarian, but it's hard for me to imagine that meat in that quantity is necessary for good health.

I just looked up where I heard about Agatston actually thinking Paleo is right diet to follow.  Here's a link to the thread where it was discussed:
http://forum.lowcarber.org/archive/index.php/t-337734.html

"It was a lecture geared towards health professionals....he spoke of how he believes in the Paleo diet(book) and that the ideal for us in our current state of evolution is a grain free diet.....really..he said that!!

He also did not know that his Meal Plan Guide is telling us to add in cereal first in phase II....he said he would get that changed...it should be berries only...first...then starchy veggies.....whole grain last and after whole grain...then processed grain ie: flour/bread :idea:

He also told me that they put whole grains into the plan so that it'd be easier for people to adapt to the plan....they know that people are addicted to grain and it would be too hard for most to give them up totally...me :wave: ;) He was trying to make the plan marketable to all and he felt that telling us to eat whole grain is better than what we were doing before...and he's right."

See, this is where I have a problem with that sort of thinking.  Instead of telling you what is optimal for your health, they tell you what they think you'll comply with instead.  I think the ADA does that too.  The results of this are that people might be slightly healthier than if you did nothing but you're a long ways off from the health you could achieve if you were fully informed at the beginning.

Some of us have the discipline to make the needed changes.  Dear Doctors, please don't assume we're all hopeless!

South Beach Diet in my opinion is awesome.  After Phase I you lose your cravings.  I have been into nutrition for over 30 years, and still need to lose a few pounds.  On this diet you eat healthy fresh foods, you don't have to eat any meat if you don't want to and if you're vegan it can work as well.

One of the great things about it is you don't have to be manic, it's pretty simple. You are full eating lots of fiber from fresh veggies.   Those foods God planned for us to eat, instead of processed and over cooked foods.

One thing you mentioned was the LPP test for heart disease, I have a question, why aren't M.D.'s requesting this test more often.  The docs who are requesting this are those who are both  N.D. M.D.'s, they look at the whole person not just one aspect.

In addition, since I have been involved with cardiac CT for now nearly 24 years, the PLC also affords me an opportunity to develop a CT coronary angiography training program for cardiologists and radiologists (www.cardiaccta.us). Together, these new efforts are merely an extension of my interests in prevention, patient care, and teaching.

Thanks for the encouragement.  I have always hoped and believed it was possible for me to control my blood pressure without medication, (without receiving much guidance or encouragement toward that goal from my physician) and while that may not be entirely possible now given my age (62) and fairly long-standing history of hypertension, I have seen good improvement in my readings since becoming stricter with lower carbohydrates, and losing about 20 pounds over 4-5 months.  In light of this topic, would you consider commenting or doing a longer post on the effects of weight loss in older people?  Jenny Ruhl had a post on DiabetesUpdate recently (August 6th, "More Evidence that Weight Loss After 65 Is Dangerous to Your Health") concerning a study that was interpreted to show that weight loss after the age of 65 can have negative impact on health and mortality.  http://www.diabetesincontrol.com/results.php?storyarticle=5975  
I have also read opinions in the past that are similar, such as that weight loss after 60 may worsen osteoporosis (sorry, unable to cite the source for that).  Judging from my personal experience, my weight loss appears to have had beneficial effects on my BP and lipid profile, but is it possible there is a hidden cost?  Ideally, of course I would have lost weight earlier, or even more ideally, never gained it in the first place, but...!  I feel now that I have maybe 10 or so more pounds to lose to be at an optimal weight, judging from the amount of remaining abdominal fat, but perhaps that is not realistic or desirable at my age.  I have not chosen a number to shoot for, but am instead assuming that by continuing to eat as I am, emphasizing adequate protein and relying more on fats than carbs for energy, getting adequate vitamin D3, and working to keep up my muscle mass, I will naturally arrive at a healthier weight, (plus,now you offer hope that the full effect on my Blood Pressure is still to come!) Surely the assumption that I am promoting my health by losing excess weight through good nutrition practices is not one that would hold true only for a younger person?

Hi,

I wasn't sure where to post this comment, but I couldn't find anything on your site about the supposed Vitamin C--CHD connection, promoted by Pauling and Rath.  Googling around has found inconclusive studies and results; some for, some neutral. Perhaps this could be a new thread.  Thanks.  Roger

To Jenny, sure adding adequate vitamin d is important but don't forget vitamine k2 (as mk-4) and maybe a decent mix of bone building minerals like boron strontium citrate oh and some b12, folic acid etc.

I saw your site first time it is good and i think you are right we can control our blood pressure without taking any medicine.keep it up.

http://weight-loss.realhealthproducts.org/

I just accros from your blog and I thought I would have to leave my first comment after reading your great article. I think Many of the people want to know on this.So ,I think this will help them a lot.
Phentermine

yes weight is directly proportional to blood pressure, more weight is dangerous for helth! HCG diet , thanks

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.” [...]